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ARTERIAL  HYPERTONUS,  SCLEROSIS 
AKD  BLOOD-PRESSURE 


ARTERIAL 

HYPERTONUS,  SCLEROSIS 

AND  BLOOD-PRESSURE 


WILLIAM   RUSSELL,  M.D.,  F.R.C.P.,  Edin. 

PHYSICIAN   TO,    AND    LECTURER   ON   CLINICAL   MEDICINE   IN,    THE 

ROYAL   INFIRMARY,    EDINBURGH  ; 

LECTURER   ON   PRACTICE   OF   MEDICINE,    FORMERLY  LECTURER   ON   PATHOLOGY^., 

SCHOOL   OF   MEDICINE,    EDINBURGH 


WITH  THIRTY-SIX  ILLUSTRATIONS  AND  PLATES 


PHILADELPHIA 

J.     B.     LIPPINCOTT     COMPANY 

EDmBURGH:   WILLIAM   GEEEN  &   SONS 
1908 


CONTEXTS 


CHAPTER  I 

THE    NORMAL   STRUCTURE   AXD   ilOVElIENTS    OF   ARTERIES 


PAGE 


Structure — Tone — Movements — Pulsatile    Movement — Tonus    and 

Hypertonus  .......         1 


CHAPTER  II 

BLOOD-PRESSURE   AXD   ITS    RELATION   TO   VESSEL    CONTRACTION 
AND   HEART   POWER 

Blood-Pressure — Determining  Factors—  Measurement  of — Physical 
Facts  regarding — Effect  of  Peripheral  Constriction  on  Blood - 
Pressure — Effect  of  Peripheral  Constriction  on  the  Heart 


CHAPTER  III 

DISEASES    OF   ARTERIES 

Introductory  —  Historical  Summary  —  Relation  of  Atheroma  to 
Arterio-sclerosis — Arteries  and  Heart  in  Granular  Kidney — 
Atheroma  and  Endarteritis  Deformans — Etiology — Obliterative 
Endarteritis  and  Acute  Aortitis — Arterio-sclerosis — Changes  in 
Arteries  of  the  Kidney  in  Arterio-sclerosis,  "  Arterio-capillaiy 
Fibrosis"— "Hypermyotroj)hy" — Conclusion      .  .  .13 


CHAPTER  IV 

HYPERTONUS    AND   ITS    CLINICAL    RECOGNITION 

Hypertonus  in  Xon-thickened  Arteries— Hypertonus  in  Sclerosed 
Vessels — Hypertonus  and  Relaxation  in  Atheromatous 
Arteries — Cases  .  .  .  .  .  .27 


CONTENTS 


CHAPTER  V 

THE   CAUSES    OF    HYPERTONIC   CONTRACTION 

PAGE 

The  Influence  of  the  Nervous  System — The  Influence  of  the  Com- 
position of  the  Blood  —  Exjaerimental  Work  —  Views  of 
Clinicians — The  "Localisation  of  the  Action"  on  the  Vessel 
Wall — Action  of  Adrenalin — Myoneural  Junction — Action  of 
Ergot — Action  of  Infundibular  Portion  of  the  Pituitary  Body — 
Influence  of  Tobacco  .  .  .  .        ,     .  .33 

CHAPTER  VI 

THE    CLINICAL   ESTIMATION    OF   BLOOD-PRESSURE 

Arterial  Tension  and  Blood -Pressaire — Methods  of  estimating  Blood- 
Pressure — Influence  of  the  Condition  of  the  Arterial  Wall — 
Factors  determining  Haemomanometer  Readings  —  Tissues 
surrounding  Arteries — Thickness  of  Arterial  Wall — The  Blood- 
Pressure  inside  the  Vessel  .  .  .  .  .43 

CHAPTER  VII 

A   NEW   SCHEMA   OF   THE   CIRCULATION 

Description  of  Schema — Eff'ect  of  Constriction  on  the  Pressure  in 
the  Tubes — Influence  of  the  Thickness  of  the  Walls  of  the 
Tubes — Result  of  High  Pressure  in  thin-walled  Tubes  .  .       56 


CHAPTER  VIII 

PRESCLEROSIS — HYPERTONUS    VERSCTS  BLOOD-PRESSURE — THE 
MODE   OP   PRODUCTION   OF   ARTERIO-SCLEROSIS 

Presclerosis  —  Views  of  Huchard,  etc. — Mode  of  Production  of 
Arterio-sclerosis — "Muscular  E.xcitants" — Result  of  Continu- 
ance of  Hypertonic  Contraction  .  .  .  .  .62 


CHAPTER  IX 

THE   PRACTICAL   APPLICATION    OF   THE   PRECEDING   CONCLUSIONS 

Resume  of  preceding  Chapters — Vessel  Sensitiveness  and  the  Clinical 
Significance  of  Hypertonus — The  Interpretation  of  Hfemomano- 
meter  Readings — Angiohsemomanometer  or  Angiomanometer    .       6"/ 


CONTENTS  vii 


CHAPTER  X 

HYPERTONUS  AS  SHOWX  BY  THE  SPHYGMOGRAPH 

TAGE 

Illustrative  Cases  showins  also  the  effect  of  Vaso-dilators      .  .       75 


CHAPTER  XI 
THE  cli:n'ical  significance  and  value  of  h^momanometer 

OBSERVATIONS   IN   ADVANCED   INTERSTITIAL   NEPHRITIS 

The  Influence  of  the  Vessel  Wall  in  Heemomanometer  Readings  in 
advanced  Interstitial  Nephritis — Illustrative  Cases — Interpre- 
tation of  the  Readings       .  .  .  .  .  .79 


CHAPTER  XII 

THE  INFLUENCE  OF  THE  ALIilEXTARY  SYSTEM  IN  CAUSING 
ARTERIAL  HYPERTONUS  AND  SCLEROSIS  :  FOOD,  DIGESTION, 
CONSTIPATION,    AND   ALCOHOL 

Current  Views  as  to  the  Influence  of  Food  and  Digestion — Physio- 
logical Phenomena  during  Digestion — Eff"ect  of  Excess  in  Diet — 
Effect  of  Intestinal  Putrefaction — Putrefaction  of  Proteids — 
Effect  of  the  Alimentary  System  on  Sclerosed  Vessels — Influence 
of  the  Alimentary  System  on  the  Adrenals — Illustrative  Cases  . 


CHAPTER  XIII 

HoEMOilANOMETER    PRESSURES   IN    CASES    OF    ACUTE    ALCOHOLISM 

Cases  of  Acute   Alcoholism  with    Low  Pressure   and   with    High 
Pressures — Effect   of   a   Vasodilator    added    to    the    ordinary 
Treatment  in  the  High  Pressure  Cases  .  .  .113 

CHAPTER  XIV 

GROUPS   OF    CASES   ILLUSTRATING   H.^iMOMANOMETER    READINGS 

Cases  of  Bright's  Disease— Miscellaneous  Cases— Cases  of  elderly  and 
aged  Persons— The  Relation  between  the  Radial  and  Brachial 
Arteries  —  Cases  with  Heart  Symptoms  —  Importance  of 
recognising  Hyper  tonus  in  Cardiac  Cases  .  .  .119 


CONTENTS 


CHAPTER  XV 

THE  RELATION  OF  AXGINA  PECTORIS  AKD  ALLIED  CONDITIONS 
TO  AN  ARTERIO-CARDIAC  REFLEX  HAVING  ITS  ORIGIN  IN  THE 
ABDOMEN,   AND   CAUSING  HYPERTONIC   CONTRACTION 

PAGI 

Introductory  —  Historical  —  Views  regarding  Angina  Pectoris — 
Angina  Pectoris  Vasomotoria  —  Intermittent  Claudication — 
Lauder  Brunton  and  Amyl  Nitrite — What  is  included  under 
"  Angina  Pectoris  "  "? — ConstructiA^e  and  Critical — An  Arterial 
Abdominal  Reflex — Exaggeration  of  Xormal  Reflex — Action  of 
Reflex  on  Sclerosed  Arteries — Relation  of  Reflex  to  Angina 
Pectoris  —  Illustrative  Cases  —  Clinical  Pathology  —  Th  e 
Unifying  Principle  ......     121 


CHAPTER  XVI 

THE   PHENOMENA   CAUSED    BY    HYPERTONIC    CONTRACTION    OR 
SPASM   CONSTRICTION   OF   CEREBRAL   ARTERIES 

Contractility  of  Cerebral  Arteries — Vessels  acted  on  by  Substances 
in  the  Blood — Application  of  this  to  Cerebral  Vessels — Nerve  In- 
fluence— Influence  of  Blood  Composition — Eft'ect  of  Strychnine 
— Relation  of  the  Pituitary  Body  to  the  Cerebral  Circu- 
lation —  Clinical  Application  —  Transitory  Phenomena  — 
Accompaniments  of  Migraine — Illustrative  Cases — Cases  with 
recurring  Mental  or  Motor  Phenomena — Cases  of  permanent 
Paralysis  or  Paresis  preceded  by  "Warning  Attacks" — -Fatal  Cases 
of  Hemiplegia — Cerebral  Softening  from  Vessel  Constriction 
versics  Htemorrhage — Case  of  Temporar}-  Paresis  accoftipanying 
Paroxysms  of  Angina  Pectoris — Case  of  old-standing  Hemi- 
paresis  with  Temporary  Complete  Right  Hemiplegia  and  Aphasia 
— Case  of  Cheyne  -  Stokes  Breathing  with  thick  Arteries — - 
Clinical  Pathology  of  the  preceding  Groups  of  Cases — Minor 
Phenomena  and  Focal  Spasm  —  The  Special  Irritant  —  The 
Phenomena  in  Persons  with  Sclerosed  Vessels — Temporary  and 
Permanent  Paralysis  in  Persons  with  Sclerosed  Vessels — 
Softening  or  Htemorrhage  ? — Symptoms  due  to  a  Feeble  Circu- 
lation— Treatment  .  .  .  .  .  .     153 


CHAPTER  XVII 

CONCLUSION 

Order  of  Links  in  Chain  of  Evidence  .....     191 


LIST   OF   ILLUSTRATIONS 


1,  2.  Sections  of  Arteries  showing  Elastic  Tissue  in  Walls  2 

3.  Section  of  Atheromatous  Artery        .             .             .  18 

4.  Do.                   do.                   with  recent  Blood  Clot  18 
5,  6,  7.  Sections  of   Atheromatous   and  Calcareous  Eadial 

Arteries  .             .                          .             .             .  20,  22 

8.  Section  of  Artery  showing  Obliterative  Endarteritis  22 
9,  10.  Sections  of  Radial  Artery  and  of  Kidney  showing 

Arterio-sclerosis  both  from  same  Case    .             .  24 
11,  12,  13.  Sections   of   Radial   and  Coronary  Artery  and  of 

Kidney  all  from  same  Case         ...  24 
14,  15.  Sections     of     Normal     Radial     Arteries     showing 

Hypertouus          .....  52 

16.  Section  of  Radial  Artery  showing  Sclerosis  .             .  52 

17.  Section  of  Sclerosed  and  Hypertonic  Radial  Artery  52 

18.  Do.  do.  do.  do. 

(pure  Hypermyotrophy)              ...  52 

19.  New  Schema  of  the  Circulation         ...  57 

20.  Transverse  Sections  of  Tubes  used  in  Schema           .  57 
21-28.  Sphygmograpliic  Tracings  illustrating  Hypertonus .  76,  77 
29,  30.  Sections     of     Radial     Arteries     showing    Hyper- 
myotrophy          .....  80 

31.  Sphygmograpliic  Tracing       ....  124 

32,  33.  Sections  of  Brain  showing  Areas  of  Softening          .  175 
34,  35,  36.  Pulse  Tracings  from  a  Patient  with  Cheyne-Stokes 

Breathing  .  .  .  .  .     179,  180 

Dr.  George    Olivei-'s  Hseniomanometer  with  Wrist 

Bag           ......  48 


CHA.PTER   I 

THE  NORMAL  STRUCTURE  AND  MOVEMENTS  OF 
ARTERIES 

STEUCTURE  :    PULSATILE   MOVEMENT ;    TONE    AND 
HYPERTONUS. 

Although  it  is  fully  recognised  that  the  nutrition  of  the 
body  as  a  whole,  and  the  vigour  of  its  component  parts  and 
organs,  depend  upon  the  blood  supply,  clinical  attention  is 
almost  wholly  directed  to  the  condition  of  the  blood  itself — 
to  the  enumeration  of  its  corpuscles  and  the  estimation  of  its 
htemoglobin  richness.  The  condition  of  the  channels  by  which 
the  blood  reaches  the  various  organs  receives  but  scant  con- 
sideration, although  it  is  only  necessary  to  mention  the  neglect 
to  make  it  apparent  that  such  neglect  carmot  be  wise.  Our 
purpose  in  these  pages  is  to  direct  attention  to  the  important 
part  taken  by  the  blood  vessels  in  the  production  of  clinical 
phenomena,  varying  in  intensity  from  trifling  indisposition  to 
severe  illness  in  which  life  is  seriously  and  often  immediately 
threatened.  The  subject  is  very  wide,  and  no  attempt  will 
he  made  to  cover  the  whole  field.  Only  those  conditions 
will  be  dealt  with  which  are  fundamental  and  specially 
illustrative. 

As  a  preliminary  to  our  investigation,  it  is  necessary  to 
recall  the  anatomical  structure  and  nervous  relations  of  the 
blood  vessels. 

Arteries  consist  of  three  coats :  the  external  coat,  or 
tunica  adventitia,  is  formed  of  connective  tissue  in  which 
there  are  nerves,  lymphatics,  vaso-vasorum,  and  in  addition 
a  considerable  layer  of  elastic  fibres  next  the  media,  not 
commonly  described  ;  the  middle  coat,  or  tunica  media,  is 
A 


PULSATILE  MOVEMENT,  TONE,  AND  HYPERTONUS 

formed  of  unstriped  muscle  fibres,  which  run  transversely  and 
thus  surround  the  vessel ;  the  internal  coat,  or  tunica  intima, 
is  formed  of  a  layer  of  polygonal  endothelial  cells  with  a  fine 
line  of  sub-endothelial  connective  tissue  underlying  them. 
In  some  of  the  arteries  there  is  an  elastic  lamina  between 
the  internal  and  middle  coats,  and  another  between  the  middle 
and  external  coats.  These  are  known  respectively  as  the 
internal  and  external  elastic  laminm  ;  they  are  by  no  means  con- 
stantly present,  and  often  only  the  internal  one  is  represented. 
In  the  large  arteries  the  middle  coat  is  made  up  to  a  great 
extent  of  elastic  fibres. 

The  arteries  are  supplied  with  nerves,  which  connect  them 
with  the  vasomotor  centre  in  the  medulla. 

The  muscular  tunic  of  arteries  has,  like  muscle  everywhere 
else,  what  is  known  as  tone  or  tonus.  This  is  a  sustained 
measure  of  contraction  of  its  individual  fibres,  which  may  be 
increased  or  diminished.  It  is  commonly  taught  that  it  is 
regulated  by  nervous  influences  conveyed  through  the  sym- 
pathetic, the  constrictor  fibres  of  which  when  stimulated  lead 
to  an  increase  of  tone,  or  even  to  a  distinct  degree  of  abnormal 
arterial  contraction ;  while  the  withdrawal  of  sympathetic 
action  leads  to  lowering  of  normal  tone,  or  to  a  definite 
relaxation  of  the  arterial  wall. 

While  the  tone  of  arteries  can  be  thus  controlled  by  the 
sympathetic,  there  is  the  authority  of  Leonard  Hill  for  the 
observation  that  it  is  soon  restored  after  section  of  the  vaso- 
motor nerves.  The  tone  under  such  circumstances  is  regarded 
by  him  as  being  then  maintained  by  the  blood-pressure.  It 
will  be  subsequently  shown  that  another  factor  has  to  be 
taken  into  consideration  when  tone  is  lowered  or  increased, 
as  it  is  in  the  disorders  which  come  under  the  notice  of  the 
physician. 

In  considering  the  movements  of  arteries,  it  is  to  be  noted 
that  they  have  firstly  a  pulsatile  movement — probably  a 
rhythmical  response  to  the  rhythmical  flow  of  the  blood, 
corresponding  with  ventricular  systole  and  diastole.  It  is 
probably  not  merely  the  stretching  and  contraction  of  an 
elastic  tube  by  a  wave  passing  along  its  contained  fluid,  but 
the  same  kind  of  unceasing  rhythmic  movement  the  heart 
possesses.     However  that  may  be,  it  is  important  to  divest 

2 


M 


Fig.  1. — Int.,  in  the  lumen  of  the  artery,  showing  near  it  the 
multiplication  of  the  internal  elastic  lamina  ;  M,  tunica  media  ; 
EF,  the  layer  of  elastic  fibres  external  to  the  tunica  media. 


Fig.  2.— The  description  to  Fig.  1  is  a^Dplicable  to  this  fio-urc  also. 


{The  sections  from  which  these  micro-photograxilis  were  taken  icere  kindly 
prepared  for  me  It/  Miss  Huie.) 


PULSATILE  MOVEMENT,  TONE,  AND  HYPERTONUS 

our  minds  of  the  current  notion  that  the  arteries  are  a  mere 
system  of  elastic  tubes. 

In  addition  to  the  pulsatile  movement,  there  is  a  further 
movement,  which  is  allied  to  tone,  and  yet  is  such  an 
abnormal  exaggeration  of  it  that  the  terms  contraction,  con- 
striction, and  spami  have  all  been  applied  to  it.  Although 
occasionally  recognised,  it  has  been  to  a  great  extent  ignored 
ill  clinical  medicine,  and  its  significance  has,  as  an  inevitable 
consequence,  been  overlooked.  The  thought  of  "  blood- 
pressure  "  has  possessed  the  field,  to  the  practical  exclusion 
of  the  arterial  wall. 

The  accentuation  of  this  normal  movement  is  of  great 
clinical  significance,  and  as  it  varies  within  wide  limits  it  is 
desirable  to  have  words  or  terms  to  express  the  differences. 
The  normal  degree  of  tonicity  varies,  and  it  varies  under 
conditions  which  are  to  be  regarded  as  normal.  It  is  there- 
fore impossible  to  do  more  than  have  a  somewhat  empirical 
nomenclature  to  define  its  variations.  What  is  of  practical 
importance  is  to  know  that  the  tonicity  does  thus  vary ; 
to  be  able  to  recognise  dift'erences  when  they  are  present, 
and  to  understand  that  such  variations  are  no  mere  chance 
phenomena  without  cause  or  significance.  The  normal  tonicity 
or  tone  is  to  be  noted  in  the  soft  vessel  of  perfect  health. 
This  tonicity  is  increased  under  physiological  conditions,  as 
during  digestion  and  during  physical  effort.  This  is  a 
physiological  hypertonus :  no  other  term  expresses  the 
fact :  it  is  an  increase  of  a  normal  state  due  to  an  increase 
in  the  intensity  of  normal  stimuli.  The  term  hypertonus 
has  sometimes  been  objected  to  since  I  introduced  it  in  this 
connection,  but  a  word  was  required  that  would  carry  the 
idea  which  has  been  indicated.  When  the  hypertonus  occurs 
in  an  artery  the  increased  measure  of  contraction  of  the 
muscular  coat,  which  is  necessarily  implied,  means  that  the 
wall  of  the  vessel  becomes  somewhat  thicker,  that  its  dia- 
meter is  somewhat  reduced,  and  its  lumen  correspondingly 
diminished.  The  degree  of  contraction  may  exceed  the  limits 
of  normal  variation,  and  when  it  does  so  the  term  hypertonic 
contraction,  or  merely  arterial  contraction,  will  be  used  here. 
The  word  contraction  has  such  a  variety  of  meaning  in 
medicine,  and  so   commonly  means  a   narrowed  orifice   or  a 

3 


PULSATILE  xMOVEMENT,  TONE,  AND  HYPERTONUS 

strictly  limited  constriction  in  a  tube,  that  it  reqnires  the 
adjective  hypertonic  to  indicate  an  effect  which  is  wider  and 
more  generalised  through  the  arterial  system.  The  term 
hypertonic  contraction  will  therefore  be  used  to  indicate 
this  greater  degree  of  arterial  constriction.  There  is  yet 
another  condition,  differing  from  the  preceding  in  being 
a  localised  constriction.  In  the  two  preceding  conditions,  the 
"hypertonns"  and  the  "hypertonic  contraction,"  the  contrac- 
tion affects  the  whole  systemic  system.  In  the  third  con- 
dition the  arterial  constriction  is  localised,  and  may  be  so 
extreme  in  degree  as  to  greatly  diminish  or  completely  shut  off 
the  blood  flow  in  the  affected  vessels  ;  to  this  condition  the  term 
arterial  sjmsm  is  most  suitably  applied,  and  will  be  confined  in 
these  pages.  It  will  from  this  be  realised  that  the  morbid  is 
but  an  exaggeration  or  an  intensification  of  the  normal  process. 
The  reverse  of  hypertonns  is  loss  or  diminution  of  tone. 

REFERENCE. 
Leonard  Hill,  Schiifer's  Physiology,  1900,  vol.  ii.  p.  138. 


CHAPTER   II 

BLOOD-PRESSURE  AND  ITS  RELATION  TO  VESSEL 
CONTRACTION  AND  HEART  POWER 

During  the  past  few  years  greatly  increased  interest  has 
been  taken  in  the  important  subject  of  blood-pressure,  and 
in  the  means  of  clinically  measuring  it.  It  is  therefore 
necessary  to  consider  certain  questions  which  have  risen  up 
around  these,  especially  those  which  are  of  clinical  importance. 
In  no  department  of  practical  medicine  is  correct  knowledge 
so  essential  for  the  satisfactory  translation  of  mental 
conception  into  practical  understanding  and  therapeutic 
application,  and  in  this  chapter  I  shall  endeavour  to  make 
this  evident. 

Blood-pressure  is  determined  by  several  factors :  first, 
by  the  driving  power  of  the  left  ventricle  ;  second,  by  the 
channels  in  which  the  blood  flows  ;  and  tliircl,  by  the  condition 
of  the  flowing  blood.  The  second  of  these  may  be  sub- 
divided ;  but  for  the  present  it  is  important  to  realise  that 
these  embrace  all  the  factors,  and  are  the  only  factors  which 
determine  the  measure  of  the  blood-pressure. 

The  blood-pressure  is,  of  course,  the  pressure  exercised  by 
the  flowing  blood  inside  the  vessels.  Physiologists  measure 
it  by  means  of  a  cannula  introduced  into  a  vessel,  and  com- 
municating with  a  manometer  outside  it.  In  this  way 
an  accurate  record  is  obtained  of  the  pressure  in  the  left 
chambers  of  the  heart,  in  the  great  arteries,  and  in  the  great 
veins  where  they  empty  their  blood  into  the  right  auricle. 
Observations  of  this  nature  are  made  on  healthy  animals. 

Certain  of  the  observations  made  on  such  a  system  of 
tubes  as  is  provided  by  the  vessels  fall  within  what  we  may 
call  the  ordinary  laws  of  physics ;  others  of  them  are  the 
result  of   the  whole   circuit,   consisting  of  living   structures, 

5 


BLOOD-PRESSURE  AND  VESSEL  CONTRACTION 

being  influenced  and  played  upon  both  by  a  nervous  system, 
and  by  the  flowing  blood  itself,  which  is  in  constant  contact 
with  it. 

Some  of  the  'pliydcal  facts  are  as  follows.  Starting  from 
the  left  ventricle,  the  blood-pressure  is  highest  in  the  aorta, 
and  falls  gradually  towards  the  capillaries,  which  may  be 
regarded  as  the  periphery.  This  is  true  of  the  flow  of  any 
kind  of  fluid  through  a  system  of  tubes.  The  fall  in 
pressure,  as  the  periphery  is  approached,  is  the  result  of 
friction  between  the  flowing  fluid  and  the  wall  of  the  tubes. 
A  thick  fluid  flows  less  readily  than  a  thin  fluid ;  in  small 
tubes  the  obstruction  is  greater  than  in  large  ones. 

In  the  circulation,  as  it  is  seen  in  living  animals,  vital 
])rocesses  have  to  be  considered,  for  they  often  determine 
physical  changes.  It  is  of  great  importance  to  separate  these 
two  sets  of  phenomena  when  circulatory  disturbances  are 
considered.  To  illustrate  this,  we  may  suppose  that,  as  the 
result  of  vital  influences,  the  vessels  in  a  considerable  area 
become  contracted,  and  the  circulation  through  them  thereby 
impeded ;  the  blood-pressure  in  the  vessels  above  the  area  of 
constriction  is  raised  as  a  necessary  consequence.  This  takes 
place  in  an  artificial  scheme  formed  of  rubber  tubes  as 
certainly  as  in  the  living  vessels.  Such  a  raising  of  pressure, 
if  it  is  sufficiently  great,  will  travel  back  to  the  aorta  ;  if  it  is 
confined  to  a  limited  area  the  increased  pressure  will  be  lost 
before  the  aorta  is  reached,  in  virtue  of  the  elasticity  of  the 
tubes.  The  mean  or  average  pressure  over  the  whole  system 
is  not  affected  so  long  as  the  driving  power  of  the  heart 
remains  undisturbed;  the  distribution  of  the  2^resstire  is, 
however,  altered, — where  the  vessels  are  constricted  the 
pressure  falls,  where  they  are  not  constricted  it  is  raised. 
The  fall  and  the  rise  balance  each  other,  and  so  the  mean 
pressure  is  not  altered.  As  has  been  said,  the  pressure  in 
the  aorta  is  often  raised  under  the  circumstances  indicated, 
and  it  is  this  fact  which  has  given  rise  to  the  dictum  that 
peripheral  constriction  or  ohstruction  raises  hlood-jjressure.  The 
dictum  would  certainly  be  found  to  occupy  an  honoured  place 
in  a  "Proverbial  Philosophy"  of  medicine,  did  such  a 
compilation  exist;  but  like  all  such  dicta,  it  is  false  as 
well  as  true,  and  it  would  demand  considerable  ingenuity  to 

6 


BLOOD-PRESSURE  AND  VESSEL  CONTRACTION 

determine  which  aspect  predominates.  In  a  limited  sense  it 
is  miimpeachable,  yet  it  has  had  the  most  unfortunate  results 
in  practical  medicine.  It  has  been  the  common  answer  to 
many  questions,  and  has  stopped  the  mouths  of  many 
inquirers  and  seekers  after  truth. 

Peripheral  constriction,  no  matter  how  caused,  raises  blood 
pressure — but  where  ?  Is  it  in  the  constricted  vessels  them- 
selves ?  Prom  much  that  has  been  written  the  question  might 
be  answered  in  the  positive,  and  yet  the  conception  is  de- 
plorably misleading  as  a  practical  guide.  The  rise  of  pressure 
is  behind  the  constriction,  and  the  physiologists  measure  it  in 
the  aorta.  The  physical  law  is  perfectly  simple  when  truly 
applied :  if  the  capillaries  constrict,  the  rise  in  pressure  is  in 
arterioles ;  if  the  constriction  includes  arterioles,  the  raised 
pressure  tells  from  the  small  arteries  backwards,  and  so  farther 
and  farther  back.  The  whole  mixed  conception  that  a  con- 
stricted vessel  has  its  blood-pressure  raised  has  to  be  abandoned 
for  a  more  accurate  and  infinitely  more  illuminating  concep- 
tion of  the  changes  w^hich  take  place. 

When  the  raised  blood-pressure  reaches  so  far  back  as  the 
aorta,  what  is  its  effect  ?  In  direct  proportion  to  the  increase 
of  pressure  in  the  aorta  is  the  increase  of  power  required  by 
the  left  ventricle  to  open  the  aortic  cusps  and  to  expel  its 
blood.  This  is  how  the  raising  of  pressure  leads  to  increased 
heart  effort.  If  the  myocardium  be  sound  it  does  this  in 
virtue  of  its  reserve  of  power,  which  is  called  out  through 
the  medium  of  the  nervous  mechanism.  The  raising  of  aortic 
blood-pressure  is  the  inevitable  'pliij&kal  consequence  of  a 
peripheral  constriction,  which  is  a  xital  phenomenon,  while 
the  response  of  the  heart  is  again  a  mtal  phenomenon.  It 
is  thus  seen  how"  essential  it  is  to  separate  mechanical  and 
vital  factors.  The  response  on  the  part  of  the  heart  is 
commonly  represented  as  intended  to  maintain  blood  pressure  ; 
it  seems  ofteii  to  be  thought  of  as  maintaining  the  pressure 
all  round.  If  the  heart  did  not  respond  there  would  be  a 
fall  in  aortic  pressure ;  but  if  it  responds  in  proportion  to  the 
rise  of  pressure  in  the  aorta,  the  mean  is  maintained,  but  the 
maintenance  of  the  mean  does  not  imply  that  an  increased 
flow  occurs  in  the  area  w^here  the  vessels  are  constricted. 
The  conception  that  the  heart  is  constantly  battling  to  meet 

7 


BLOOD-PRESSURE  AND  VESSEL  CONTRACTION 

the  cry  of  the  tissue  cells  for  a  sufficient  blood  supply,  as  a 
mother  tends  her  young,  is  a  very  pretty  conception,  but  is 
disproved  by  many  morbid  processes.  What  the  heart  has 
to  cope  with  is  the  enemy  at  its  gate — the  mechanical 
difficulty  of  raised  aortic  pressure ;  and  I  question  if  the 
heart  does  more  than  overcome  that. 

The  circulation  as  a  living  scheme  has,  however,  more 
than  one  way  by  which  the  heart  can  be  saved  from  the 
strain  of  such  a  change  as  has  been  indicated.  If  the 
systemic  system  be  constricted  the  splanchnic  area  may 
dilate,  and  thus  ease  aortic  pressure.  The  heart  itself  has 
its  regulating  mechanism,  so  that,  if  the  aortic  pressure  be 
more  than  it  can  completely  overcome,  an  increase  of  residual 
blood  in  the  ventricle  leads  to  over-distension,  which  so  affects 
the  vagus  terminals  that  the  heart  is  slowed,  and  the  blood 
is  given  more  time  to  pass  through  the  constricted  vessels. 
If  the  splanchnic  area  be  dilated,  as  during  digestion,  the 
systemic  vessels  commonly  become  somewhat  constricted, 
doubtless  to  adapt  themselves  to  the  determination  of  so 
large  a  volume  of  blood  to  the  abdomen.  This  maintains 
aortic  pressure,  which  might  be  dangerously  lowered  by  the 
sudden  influx  of  blood  to  the  splanchnic  area :  to  regard  the 
condition  in  the  systemic  vessels  as  a  raising  of  blood-pressure 
to  provide  the  tissues  supplied  by  the  systemic  vessels  with 
sufficient  pabulum,  is  one  of  the  most  curious  of  the  concep- 
tions whicli  adorn  this  subject. 

There  is  another  aspect  of  the  circulation  which  must 
be  kept  in  view  when  considering  the  effect  which  peri- 
pheral changes  have  upon  the  heart,  namely,  this,  that  when 
the  flow  at  the  periphery  is  diminished,  from  constriction  of 
the  vessels,  blood  tends  to  accumulate  on  the  venous  side ; 
less  blood  then  reaches  the  heart,  and  the  output  of  the 
heart,  as  is  well  known,  is  dependent  in  part  on  the  amount 
which  flows  into  it.  It  is  equally  well  known  that  the 
venous  system  can  hold  all  the  blood  in  the  body,  that, 
indeed,  the  splanchnic  vessels  themselves  can  do  so  to  such 
an  extent  that  it  is  said  a  man  can  be  fatally  bled  into  his 
splanchnic  vessels. 

It  has  therefore  to  be  kept  clearly  in  mind  that  the  vital 
side  of  the  circulation  provides  abundant  means  for  easing  off 

8 


BLOOD-PRESSURE  AND  VESSEL  CONTRACTION 

aortic  pressure  when  it  threatens  to  become  excessive,  and 
that  even  on  a  priori  grounds  the  enormous  increases  in  so- 
called  blood-pressure  which  are  recorded,  at  once  ought  to 
arouse  the  suspicion  that  there  has  been  something  wrong  in 
the  method  of  examination,  or  in  the  interpretation  of  tlie 
records  obtained. 

When  systemic  hypertonic  contraction  occurs,  the  radial 
arteries  participate  in  the  contraction,  and  this  contraction  is 
commonly  regarded  as  "  raised  blood  -  pressure," — an  error 
which  owes  its  origin,  iirstly,  to  the  ignoring  of  the  fact  that 
the  arteries  are  contracted ;  and  secondly,  to  the  conception 
that  the  rise  in  blood-pressure  which  occurs  in  the  aorta 
means  a  rise  of  pressure  in  the  radials  also. 

In  some  circumstances,  which  will  be  dealt  wdth  later, 
it  can  most  reasonably  be  assumed  that  the  general  con- 
striction of  vessels  which  occurs  is  for  the  purpose  of  saving 
the  tissues  from  an  impure  blood ;  while  on  the  other  hand, 
did  we  regard  the  successfully  struggling  heart  as  stimulated 
by  the  nutritional  needs  of  the  tissues,  we  should  have  to 
accept  the  existence  of  two  antagonistic  processes,  main- 
taining an  internecine  strife  for  supremacy  —  the  arteries 
exercising  the  right  to  protect  the  tissues,  the  heart  heed- 
lessly insisting  on  forcing  through  the  impure  and  hurtful 
blood.  And  yet  it  seems  to  me  as  if  much  that  has  been 
written  on  the  subject,  say,  of  granular  kidney,  had  this 
underlying  conception  for  its  inspiration. 

The  position  comes  to  be  this — that  peripheral  con- 
striction raises  aortic  blood-pressure,  and  unless  this  can  get 
relief  by  dilatation  and  an  increased  flow  in  another  peripheral 
area,  the  heart  requires  increased  power  to  overcome  the 
increased  aortic  pressure.  The  conception  of  increased 
pressure  in  the  constricted  area,  to  be  correct,  would  imply 
a  heart  effort  of  great  magnitude,  while  all  that  the  heart  is 
really  called  upon  to  do  is  to  empty  its  left  ventricle  contents 
into  the  aorta,  the  pressure  in  which  while  heightened  can 
be  eased  off  and  relieved  in  the  ways  already  referred  to. 

For  the  heart  to  successfully  cope  with  increase  of  aortic 
pressure,  it  has  the  reserve  of  power  which  has  been  already 
referred  to.  This  is  well  and  fully  recognised.  The  exercise 
of  this  reserve  leads  in  favourable  conditions  to  heart  hyper- 

9 


BLOOD-PRESSURE  AND  VESSEL  CONTRACTION 

trophy ;  but  it  has  l3een  wisely  insisted  upon  by  Broaclbent 
and  others  that  the  very  existence  of  hypertrophy  implies 
that  part  of  the  reserve  has  already  been  drawn  upon,  and 
therefore  that  the  hypertrophied  heart  has  less  reserve  than 
the  non-hypertrophied  one.  In  practical  medicine  we  can  go 
further  than  this,  for  it  is  equally  well  known  that  the  reserve 
of  power  is  often  very  small,  and  may  be  almost  absent.  In 
some  instances  the  response  to  a  call  for  even  a  little  extra  work 
may  be  followed  by  an  exhaustion  so  extreme  as  to  be  fatal. 

The  left  heart,  in  such  myocardial  degenerations  as  cloudy 
swelling,  fragmentation,  fatty  degeneration,  acute  and  chronic 
interstitial  carditis,  not  only  possesses  a  low  driving  power,  but 
any  reserve  it  has  is  of  the  most  flimsy  character.  This  is 
shown  by  the  embarrassment  caused  by  the  slightest  movement, 
in  extreme  cases  ;  by  the  disturbances  of  the  circulation  which 
accompany  gastric  digestion,  or  any  burden  thrown  upon,  or 
any  disturbance  of,  the  alimentary  tract. 

In  the  right  heart  not  only  do  the  changes  just  mentioned 
occur,  but  it  is  in  addition  the  special  site  of  fatty  infiltration. 
This  lowers  the  normal  reserve  of  the  right  ventricle,  so  that 
any  pulmonary  difficulty  or  physical  effort  may  suddenly  over- 
w^helm  it. 

In  the  normal  sound  animal,  including  man,  increased 
strain  calls  out  the  reserve,  and  increased  work  is  done. 
Every  clinician,  however,  knows  that  the  strain,  to  be  suc- 
cessfully endured,  depends  upon  the  condition  of  the  individual 
heart.  It  is  common  enough  to  see  persons  who  have  over- 
taxed their  hearts,  in  w^hom  the  strain  has  exceeded  the 
reserve,  with  the  result  that  dilatation  occurs,  and  the  heart 
is  promptly  placed  on  a  lower  energy  level  than  it  previously 
occupied.  In  the  first  half  or  so  of  life,  the  period  of  greatest 
physical  activity,  this  over-strain  is  rarely  immediately  fatal ; 
but  in  the  second  half  of  life  the  risk  is  greater,  and  as  life 
advances  the  danger  becomes  more  urgent.  This  effect  of 
age  upon  the  circulation  is  universally  recognised ;  but  while 
this  is  so  it  is  important  to  emphasise  the  fact  that  the 
myocardium  differs  greatly  in  individuals  of  the  same  age 
from  youth  onwards.  This  means,  of  course,  that  in  different 
persons,  at  the  same  period  of  life,  the  heart  reserve  varies 
within  wide  limits,  so  that  the  general  proposition  that  the 

lO 


BLOOD-PRESSURE  AND  VESSEL  CONTRACTION 

heart  rises  to  the  strain  put  upon  it  has  in  the  iudividual  at 
every  period  of  life  its  Hmitations  and  qualifications.  Seeing 
that  the  measure  of  the  normal  or  sound  state  varies  with 
the  individual,  it  follows  that,  while  the  physiological  principle 
holds,  the  function  of  the  physician  is  to  estimate  the  power, 
and  the  probable  reserve  of  power,  in  the  individual ;  and  to 
recognise  the  effects  of  over-strain,  however  brought  about. 
In  this  estimation  it  is  necessary,  indeed  essential,  to  keep 
the  two  factors  embraced  in  the  problem  always  before  us  : 
the  first  is  the  work  to  be  done,  which  constitutes  the 
obstruction  from  the  standpoint  of  the  circulation ;  and, 
second,  the  power  to  do  the  work,  which  is  synonymous  with 
the  driving  power,  and  the  reserve  of  power,  of  the  ventricle, 
on  which  the  strain  is  mainly  thrown.  The  problem,  while 
always  presenting  the  same  equation,  requires  that  the  value 
of  its  terms  be  determined  in  every  individual  instance.  It  is 
herein  that  both  the  difficulty  and  the  interest  of  the  physician's 
work  lies  ;  and  herein  is  one  illustration  of  how  the  physician, 
while  using  the  physiologist's  work,  may  branch  off  from  him. 
It  has  been  seen  how  the  general  proposition  is  true,  that 
when  extra  strain  is  thrown  upon  the  heart  it  responds  by 
extra  work ;  and  yet  how  that  proposition  has  to  be  modified 
and  limited  by  clinical  observation.  The  extra  strain  upon  the 
heart,  it  may  be  presumed,  comes  as  a  rule  through  changes 
in  the  vessels.  Any  increase  of  resistance  in  the  vessels,  no 
matter  how  produced,  leads  to  extra  strain  on  the  heart. 
Two  factors  may  he  regarded  as  possibly  causing  increased 
resistance :  the  first  is  change  in  the  condition  of  the  circu- 
lating blood.  An  increase  in  its  viscosity  or  specific  gravity 
would  certainly  impede  its  passage  through  the  capillaries  : 
but  we  have  on  this  point  little  or  no  knowledge  which  is  of 
practical  value,  and  seeing  that  fluid  so  readily  passes  into 
and  out  of  the  blood,  it  is  very  doubtful  whether  it  will  be 
found  to  be  a  factor  of  any  appreciable  practical  importance. 
The  second  factor  leading  to  increased  resistance  is  an 
alteration  in  the  blood  channels  themselves.  Any  narrowing 
of  their  calibre  is  undoubtedly  a  cause  of  resistance.  That 
they  do  so  narrow  is  also  l^eyond  question,  although  the 
importance  of  the  fact  has  hitherto  been  obscured  by  the  one- 
sided attention  and  devotion  to  the  vessels  as  a  mere  system 

1 1 


BLOOD-PRESSURE  AND  VESSEL  CONTRACTION 

of  elastic  tubes.  Seeing  the  resistance  lies  in  the  vessels 
themselves,  the  clinical  problems  with  which  we  propose  to 
deal  will  be  considerably  simplified.  In  the  normal  state  this 
narrowing  of  the  vessels  calls  out  the  necessary  extra  work 
from  the  heart  needed  to  overcome  the  increased  pressure 
which,  as  we  have,  seen,  occurs  in  the  aorta  ;  this  is  the  normal 
response  of  extra  work  to  extra  strain  on  the  part  of  the 
heart.  Upon  our  conception  of  what  constitutes  the  extra 
work  so  brought  out,  much,  it  will  be  seen,  depends.  The 
circumstances  we  are  at  present  considering  are  the  resistance 
offered  by  a  constricted  set  of  vessels  on  the  one  hand,  and 
a  left  ventricle  with  the  ordinary  amount  of  blood  to  empty 
itself  of  on  the  other.  With  these  premises  it  follows  that 
if  the  heart  has  sufficient  reserve  to  do  this  the  increased 
pressure  in  the  aorta  will  be  maintained.  If,  on  the  other 
hand,  the  heart  has  not  the  necessary  reserve  the  ventricle  is 
not  emptied  by  systole ;  and  if  in  any  degree  it  fails  to  empty 
itself,  the  blood  -  pressure  in  the  aorta  is  correspondingly 
lowered.  I  do  not  think  there  is  any  other  true  picture  of 
what  takes  place  under  the  circumstances  with  which  we  are 
dealing,  and  which  are  of  common  and  ordinary  occurrence. 

We  may  go  a  step  further,  with  apparently  equal  safety, 
and  say  that  in  certain  states  of  the  myocardium  it  is  incon- 
ceivable that  the  heart  can  do  the  extra  work  necessary  to 
raise  the  blood-pressure.  With  tlie  enfeebled  heart  of  debility, 
with  the  degenerated  heart  of  antemia,  how  is  it  possible  to 
have  a  raised  blood-pressure  in  the  only  sense  in  which  raised 
blood-pressure  is  of  practical  value  to  the  clinician  ? 

It  is  necessary  to  lay  stress  upon  the  contention  that  to 
the  clinician  the  all-important  factor  in  questions  of  blood- 
pressure  centres  in  the  heart.  When  the  vessels  constrict  in 
one  region,  the  heart  may  be  so  powerful  that  the  danger  is 
vessel  rupture  in  another ;  on  the  other  hand,  the  heart  may 
be  so  feeble  that  there  is  imminent  risk  of  syncope.  With 
incomplete  conceptions  of  "  peripheral  resistance  "  and  "  blood- 
pressure  "  the  central  factor  may  be  obscured.  Whatever 
tends  to  lead  away  from  this  view  of  the  circulation,  and 
whatever  methods  tend  to  obscure  this  aspect  of  it  require  to 
be  employed  with  great  caution.  This  matter  will,  however, 
be  dealt  with  more  fully  later. 

12 


CHAPTER   III 
DISEASES  OF  ARTERIES 

INTRODUCTOEY  : 

ATHEROMA ENDARTERITIS  DEFORMANS  : 

OBLITERATIVE  ENDARTERITIS ^AORTITIS  : 

CALCAREOUS  INFILTRATION  OF  TUNICA  MEDIA  : 
ARTERIO- SCLEROSIS. 

INTRODUCTOEY. 

The  difficulty  which  presents  itself  when  diseases  of  the 
arterial  wall  have  to  be  considered  is  to  be  attributed  to 
the  names  used  to  designate  the  conditions  met  with,  and 
the  confusion  which  exists  between  clinical  observations, 
pathological  teaching,  and  the  terms  used.  In  illustration 
of  this  it  is  only  necessary  to  recall  the  fact  that  in  Britain 
and  elsewhere  the  term  atheroma  was  used  to  denote  per- 
fectly definite  pathological  changes  in  vessels,  while  clinically 
it  was  commonly  applied  to  all  thickenings  of  arteries 
examined  for  clinical  purposes.  The  artery  mainly  examined 
was,  of  course,  the  radial  artery,  and  the  condition  of  it 
came  to  be  regarded  as,  in  great  measure,  an  index  of  the 
state  of  other  arteries  throughout  the  body.  It  was,  how- 
ever, known  that  the  condition  of  the  radial  artery  was 
not  a  certain  index  of  the  condition  of  the  cerebral  or  of 
the  coronary  arteries — there  was  no  invariable  relationship 
— yet  the  relationship  was  sufficiently  constant  to  warrant 
considerable  clinical  importance  being  laid  upon  changes  in 
it.  It  is  quite  within  the  limits  of  accuracy  to  say  that 
all  changes  in  the  radial  artery  were  spoken  of,  and 
thought  of,  as  atheroma ;  and  that  atheroma  was  mentally 
pictured  as  a  thickening  with  degeneration  pi    the  arterial 

13 


DISEASES  OF  ARTERIES 

wall.  In  fact,  the  conception  was  that  of  a  degenerative 
thickening.  It  was  further  universally  held  that  atheroma 
necessarily  implied  a  rigidity  of  the  artericd  wall,  and  a  loss 
in  its  elasticity.  As  a  result  of  this  line  of  thinking,  based 
ujDon  incomplete  pathological  observations,  thickened  arteries 
were  regarded  as  atheromatous  arteries,  and,  as  atheromatous 
arteries  were  rigid  arteries,  therefore  all  thickened  arteries 
were  rigid, — such  was  the  common  reasoning. 

Comparatively  recently  there  was  introduced  from  Germany 
the  term  arteriosclerosis,  which  has  been  applied  by  the 
Germans  as  widely  as  the  term  atheroma  has  been  applied 
in  this  country.  They,  however,  distinguished  between  a  local 
or  nodular  and  a  diffuse  arterio-sclerosis.  As  etymologic- 
ally  the  term  means  a  hardening  or  induration  of  the  arterial 
wall,  it  is  applicable  to  nearly  all  forms  and  varieties  of 
arterial  disease.  From  this  standpoint  there  is  no  fault 
to  find  with  it,  but  its  introduction  did  not  help  the  clinical 
position,  for  the  new  term  simply  replaced  the  older  one, 
without  carrying  any  more  precise  pathological  conception 
with  it.  It  was  rapidly  attaining  much  the  same  position 
as  "  that  blessed  word  Mesopotamia  "  had  in  •  the  Highland 
woman's  scheme  of  theology. 

In  1901,  when  my  first  paper  deahng  with  this  subject 
was  published,  I  gave  a  short  historical  summary  of  the 
position,  which  I  may  include  here.  Twenty  years  ago  the 
term  arterio-sclerosis  was  so  unknown  to  British  medical 
terminology  that  it  was  not  even  mentioned  in  the  two 
admirable  text-books  published  about  that  time  respectively 
by  Bristowe  and  by  Fagge.  Going  fourteen  years  further 
back,  Dr.  Noel  Gueneau  de  Mussy  wrote  a  historical  resume 
entitled  Etude  Clinique  sur  les  Indurations  des  Artercs ;  this 
term  induration  included  atheroma.  The  term  arterio- 
sclerosis is,  as  has  been  said,  of  German  origin,  and  the 
German  pathologists  and  clinicians  certainly  apply  it  to 
atheroma.  Ziegler,  after  saying  that  sclerosis  in  an  artery 
implies  the  existence  of  local  thickening  of  its  inner  coat, 
proceeds  to  describe  typical  atheroma.  At  the  same  time, 
he  did  not  confine  the  term  to  atheroma,  for  he  also  noted 
that  the  renal  arteries  and  their  branches  in  aged  people 
are  very  frequently  the  seat  of  sclerotic  changes,  which  may 

14 


INTRODUCTORY 

simultaneously  affect  the  arteries  of  other  regions  also,  or 
be  confined  to  the  kidney.  In  this  condition  the  intima 
of  the  arteries  was  notably  thickened,  and  the  lumen  corre- 
spondingly narrowed  or  even  obliterated ;  and  he  showed 
that  this  vascular  change  in  the  kidney  gave  rise  to  a 
special  form  of  contraction  of  the  organ,  which  he  termed 
arteriosclerotic  atrophy. 

Of  all  the  German  work,  however,  there  can  be  no 
question  that  it  was  Thoma's  which  specially  influenced 
opinion  in  this  country  and  in  America.  To  borrow  a  term 
from  social  life,  he  may  be  said  to  have  "  set  the  fashion  "  in 
the  use  and  interpretation  of  the  term  in  clinical  medicine,  and, 
so  far  as  we  have  been  able  to  find,  pathology  has  not  let  its 
voice  be  heard  beyond  the  lecture-room.  Thoma's  views  may 
be  briefly  summarised  as  follows :  the  elasticity  of  the  vessel 
wall  becomes  reduced  in  general  diseases,  acute  and  chronic 
infective  diseases,  long-continued  disturbances  of  general 
nutrition,  by  many  poisonous  substances,  and  by  functional 
overstraining  of  arteries  from  an  increase  of  the  heart's  action. 
As  a  result  the  lumen  dilates  and  the  blood  stream  is  retarded 
in  the  widened  vessel.  This  retardation  is  the  cause  of  a  new 
formation  of  connective  tissue  in  the  intima  of  the  widened 
artery.  "  The  new  formation  of  connective  tissue  in  the  intima 
renders  the  vessel  wall  more  firm,  so  that  it  appears  more 
rigid  and  less  yielding  (arterio- sclerosis,  phle])o-sclerosis, 
angio-sclerosis)."  In  short,  Thoma  holds  that  the  thickening 
of  the  intima  is  secondary  to  a  dilatation  of  the  vessel,  and 
consequent  on  slowing  of  the  l^lood  stream ;  that  the  thicken- 
ing is  to  compensate  for  the  assumed  widening,  and  to  restore 
the  equilibrium  between  lumen  and  contained  blood  which 
had  been  lost.  By  this  means,  he  maintains,  the  rapidity 
of  the  blood  flow  is  re-established. 

If  we  turn  to  the  French  school  we  find  Lancereaux 
in  189  3  writing  on  "  L'Endarterite  ou  Arterio-sclerose 
Generalisee."  He  defines  the  conditions  as  a  proliferation 
of  the  cells  of  the  intima,  which  goes  on  to  fatty  degeneration 
due  to  failure  of  nutrition.  Huchard  mentions  the  fact  that 
German  authors  always  use  the  term  arterio-sclerosis  to  signify 
atheroma  of  arteries,  and  he  asks  whether  the  terms  are 
absolutely  synonymous.     His  answer  is  in  the  negative.      He 

15 


DISEASES  OF  ARTERIES 

uses  the  term  to  designate  a  general  condition  of  which 
atheroma  is  only  one  of  numerous  manifestations.  These 
include  visceral  scleroses — all  dominated  by  a  primary  chronic 
inflammation  of  the  small  vessels  described  by  many  authors 
as  obliterative  endarteritis  (or  endarteriolitis).  Arteritis  of 
the  small  vessels,  in  short,  he  considers  the  anatomical 
characteristic  of  arterio-sclerosis  (p.   96). 

Turning  to  English  works  of  recent  date,  it  is  not  necessary 
to  go  beyond  the  valuable  System  of  Medicine  which  has  been 
edited  by  Professor  T.  Clifford  Allbutt.  Here  we  look  for  a 
true  representation  of  contemporary  medicine,  and  in  Dr 
F.  W.  Mott  we  find  an  exponent  of  the  German  view  of 
arterio-sclerosis  and  an  adherent  to  Thoma's  views  which  have 
already  been  referred  to.  He  places  the  term  "  arterio- 
sclerosis "  as  the  title  of  the  section,  and  in  the  introduction 
to  the  sul^ject  he  says  that  the  term  "  is  applied  rather  loosely 
to  a  thickening  of  the  vessel  wall.  It  includes  the  obvious 
naked-eye  change  in  the  large  arteries,  named  by  some  authors 
atheroma ;  by  others,  endarteritis  deformans.  It  includes 
also  arterio-capillary  fibrosis,  a  change  first  described  by 
Gull  and  Sutton  in  the  walls  of  the  small  vessels,  which  only 
becomes  obvious  on  microscopic  examination."  At  page  320 
he  gives  as  his  definition  of  arterio-sclerosis,  "  a  local  or 
general  thickening  of  the  arterial  wall  with  loss  of  elasticity, 
occasioned  mainly  by  fibrous  overgrowth  of  the  tunica  intima, 
secondary  and  proportional  to  weakening  of  the  muscular  and 
elastic  elements  of  the  media."  It  seems  quite  clear  that  Dr 
Mott  includes  atheroma  under  the  term  arterio-sclerosis,  and 
he  follows  Thoma  in  asserting  that  the  primary  change  in 
atheroma  is  to  be  found  in  a  degeneration  of  the  tunica  media, 
and  that  the  thickening  of  the  tunica  intima  is  secondary 
and  compensatory  to  this.  He  holds  with  Thoma  that  the 
observations  made  by  the  latter  on  paraffin  moulds  of  the 
aorta  prove  this,  without  apparently  seeing  that  these  moulds 
may  with  equal  justice  be  held  to  prove  that  the  atrophy  of 
the  media  is  secondary  and  complementary  to  the  hypertrophy 
of  the  intima.  It  is  not  my  purpose  at  present  to  elaborate 
this  point,  but  I  would  indeed  be  surprised  to  find  that 
British  pathologists  held  this  to  be  the  order  of  events  in 
atheroma. 

i6 


INTRODUCTORY 

Passing  from  this  question  of  the  inclusion  of  atheroma  in 
arterio-sclerosis,  we  find  that  Dr  Mott  describes  a  "  diffuse 
arterio-sclerosis  "  (p.  329)  in  which  the  changes  begin  in  the 
small  arteries  and  capillaries,  es^Decially  those  of  the  renal 
cortex,  brain,  and  heart,  and  are  frequently  associated  with 
"  nodular  atheroma  "  of  the  aorta.  He  says  that  "  on  minute 
examination  the  muscle  fibres  of  the  media  show  hyahne 
swelling,  fatty  degeneration,  or  atropine  changes,  so  that  the 
muscular  elements  are  often  not  recognisable  ;  this  is  especially 
the  case  in  the  small  arteries  of  the  kidney,  where  the  wall 
of  the  vessel  may  appear  to  consist  of  a  homogeneous  hyaline 
tissue.  Sometimes  the  degenerated  atropliied  fibres  of  the 
media  can  be  made  out,  but  nothing  of  the  elastic  lamina,  the 
intima  being  thickened  and  represented  only  by  a  homogeneous 
hyahne  material  with  but  few  nuclei.  The  result  of  these 
widespread  changes  is  increased  resistance  to  flow  of  blood 
through  the  capillaries,  hypertrophy  of  the  left  ventricle, 
dilatation  of  larger  arteries  from  degenerative  changes  in 
muscular  and  elastic  tissues  of  the  media,  slowing  of  the 
circulation,  and  compensatory  proliferation  of  the  subendo- 
thelial  layer  of  the  inner  coat"  (p.  330).  Here,  again, 
Dr  Mott  strongly  commits  himself  to  Thoma's  view.  In 
America,  Osier,  Councilman,  and  others,  have  committed 
themselves  to  Thoma's  views. 

From  this  risume,  which  may  be  taken  as  fairly  repre- 
sentative of  authoritative  views,  it  is  seen  that  the  term 
arterio-sclerosis  is  apphed  to  three  conditions — (1)  To 
atheroma;  (2)  to  a  generalised  endarteritis;  and  (3)  to  a 
thickening  of  the  intima,  compensatory  to  dilatation  of 
vessels  from  weakening  of  their  middle  coat. 

This  resume  could  not,  however,  be  regarded  as  even 
approximately  complete  without  reference  to  various  views 
on  the  relations  between  granular  kidney  and  the  changes 
in  the  arteries  and  heart  which  accompany  granular  kidney. 
In  fact,  no  exposition  of  arterial  changes  could  suitably  ignore 
this  side  of  the  question. 

George  Johnson  (1850—1873)  was  the  first  to  show  that 

thickening   of   the  muscle   coat   of   the  arteries  occurred  in 

granular  kidney,  and  he  held  that  the  changes  in  the  heart 

and  vessels  were  secondary  to  primary  kidney  changes.      Gull 

B  17 


DISEASES  OF  ARTERIES 

and  Sutton  (1872—1877)  propoimded  the  view  that  there 
occurred  a  generalised  change  or  disease  in  the  vessels,  to 
which  they  gave  the  name,  "  arterio-capillary  fibrosis."  The 
changes  in  the  kidney  were  regarded  as  secondary  to  this 
vessel  fibrosis.  Dickinson  (1875)  held  that  a  growth  of 
fibrous  tissue  in  the  kidney  was  the  primary  change  and  that 
the  changes  in  the  vessels  were  secondary  to  this.  Eosenstein 
(1881)  agreed  with  Johnson  as  to  the  thickening  of  the 
muscular  coat  of  the  arteries,  but  thought  that  the  thickening 
of  the  iutima  was  inflammatory.  Ewald  (1881)  held  that 
there  were  two  forms  of  changes  in  the  vessels  connected  with 
Bright's  disease — first,  that  in  which  the  kidney  was  affected 
primarily  and  was  followed  by  hypertrophy  of  the  heart  and 
of  the  muscle  coat  of  the  arteries;  and,  second,  that  in  which 
disease  of  the  general  vascular  system  was  the  starting-point 
of  the  kidney  disease.  In  this  latter  there  was  arterio- 
capillary  fibrosis,  both  in  the  kidney  vessels  and  in  the  general 
vascular  system.  He  thought  that  it  was  a  question  whether 
such  cases  should  be  called  "  Bright's  disease "  or  not. 
Dreschfeld  and  Mahomed  (1881)  held  practically  the  same 
view  as  Ewald,  the  latter  holding  in  addition  that  there  might 
be  cardio-vascular  changes  without  necessarily  renal  changes 
being  present  in  all.  Dr.  Samuel  AVest  carried  the  discussion 
down  to  1906,  and  discourses  on  the  old  theme  as  to  whether 
the  kidney  lesion  or  the  arterial  change  is  the  first  to  appear. 
He  enters  a  protest  against  granular  kidney  being  considered 
partly  under  vessels  and  partly  under  kidney. 

Having  thus  outlined  the  state  of  opinion  and  belief,  we 
may  now  tm'n  to  the  consideration  of  the  pathological 
changes  occurring  in  arteries  which  are  of  practical  import- 
ance to  the  clinician ;  and  I  shall  deal  with  these  in  the 
following  order : — 

1.  Atheroma — endarteritis  deformans. 

2.  Obliterative  endarteritis — acute  aortitis. 

3.  Calcareous  infiltration  of  the  tunica  media. 

4.  Arterio-sclerosis. 

I  adopt  this  order,  as  the  first  three  conditions  have 
been  long  known  and  taught  in  this  country,  while  the 
fourth  is  practically  a  new  entity,  and  the  one  which  is 
mainly  treated  of    in    this    book.      I    adopt    and    annex    the 

i8 


Fig.  3. — Atheromatous  artery  (  x  15).  I,  the  thickened  and 
atheromatous  tunica  intima  ;  M',  the  atrophied  media  correspond- 
ing to  the  atheromatous  part ;  M,  the  hypertrophied  tunica  media, 
where  there  is  no  atheroma. 


Fig.  4.— Atheromatous  artery  (  X  16).  I,  thickened  and  athero- 
matous intima  ;  M,  hypertrophied  media  ;  M',  atrophied  media  ; 
EL,  internal  elastic  lamina  ;   B,  recent  blood  clot. 


ATHEROMA  AND  ENDARTERITIS  DEFORMANS 

term  "  arterio-sclerosis,"  as  it  is  already  in  use,  and  as  it 
is  imdesiraljle  to  multiply  terms.  To  my  mind  it  is  quite 
reasonable  to  give  a  new  term  a  limited  application  while 
declining  to  acquiesce  in  its  displacing  older  and  more  definite 
terms. 


ATHEROMA  AND  ENDARTERITIS  DEFORMANS. 

Atheroma  is  a  focal  or  patchy  affection  of  arteries.  It 
is  characterised  by  a  local  thickening  and  degeneration  of 
the  tunica  intima.  The  thickening  consists  of  a  hyperplasia 
of  the  subendothelial  connecti\"e  tissue.  It  is,  however, 
early  associated  with  an  atheromatous  degeneration  in  parts 
of  this  thickened  intima.  The  atheromatous  change  is  a 
fatty  degeneration,  commonly  most  marked  in  the  deeper 
part  of  the  thickened  tunic.  The  atheromatous  material 
may  become  the  seat  of  more  or  less  calcareous  deposition. 
At  the  part  corresponding  to  these  changes  the  tunica 
media  is  thinned  and  atrophied,  or  may  even  show  areas 
of  necrosis  in  the  large  arteries,  as  demonstrated  by  Cowan 
and  others.  When  these  changes  are  still  further  advanced 
and  are  present  in  the  large  arteries,  they  lead  to  so 
much  deformity  that  the  term  endarteritis  deformans  was 
applied  to  them  by  the  older  pathologists.  In  the  large 
arteries,  in  addition  to  the  changes  mentioned,  there  may  be 
found  atheromatous  cysts,  atheromatous  ulcers,  calcareous  plates 
(the  result  of  calcareous  deposition  in  extensive  atheromatous 
areas),  and  local  sacculations  or  bulgings,  the  result  of 
yielding  of  parts  of  the  arterial  wall  Ijefore  the  blood- 
pressure  following  upon  the  atrophy  or  even  destruction 
of  the  tunica  media.  The  changes  may  be  so  extreme, 
and  may  so  affect  the  arch  of  the  aorta  for  instance, 
that  it  may  be  much  dilated,  a  state  of  matters  to  which 
the  term  aneurismal  dilatation  is  appKed.  Similar  changes 
affecting  a  localised  area  of  the  aorta  give  rise  to  a 
definite  aneurism. 

It  is  however  as  atheroma  affects  smaller  vessels  that  we 
are  specially  concerned  here ;  so  it  requires  somewhat  more 
consideration.  The  condition  is  very  common  in  the  cerebral 
and  in  the  coronary  arteries,  but  is  comparatively  rare  in  the 

19 


DISEASES  OF  ARTERIES 

radials.  Wherever  it  is  present  it  may  give  rise  to  local 
bulging  of  the  vessel  wall,  but  such  bulgings  do  not  necessarily 
imply  a  yielding  of  the  wall.  The  walls  at  the  affected  points 
are  usually  much  thickened  and  the  lumen  is  often  greatly 
encroached  upon,  lessening  in  a  very  important  degree  the 
•blood  channel.  The  thickening  never  uniformly  affects  the 
whole  circumference  of  the  vessel  ;  it  is  always  asymmetrical ; 
it  only  affects  small  areas ;  it  never  uniformly  affects  long 
stretches  of  an  artery,  although  there  may  be  many  areas 
closely  placed  to  one  another.  It  thus  differs  entirely  from 
the  condition  to  be  described  as  arterio-sclerosis. 

Etiology  of  Atheroma. — Atheroma  is  thus  a  focal 
affection  of  the  arterial  wall,  affecting  separate  and  limited 
areas.  The  changes  indicate,  not  only  points  or  areas  of 
irritation,  but  an  irritation  associated  with  degeneration,  and 
it  is  this  association  which  characterises  atheroma.  The 
combination  is  what  we  expect  to  find  produced  by  a  micro- 
organismal  cause.  The  theory  that  the  degeneration  is  the 
result  of  impaired  nutrition,  due  to  obliteration  of  vasa 
vasorum,  is  quite  untenable,  for  the  following  reasons,  namely, 
that  the  degeneration  often  appears  early  when  there  is  but 
slight  thickening  of  the  iutima ;  the  vasa  vasorum  may  not 
be  obliterated ;  and  in  obliterative  endarteritis  no  such 
degeneration  occurs,  although  the  intima  may  be  much 
thicker  and  the  vasa  vasorum  be  markedly  affected.  Dr.  John 
Cowan  of  Glasgow  has  made  some  interesting  researches,  from 
which  he  contends  that  atheroma  may  apparently  be  due  to 
a  number  of  conditions  in  which  micro-organismal  infection 
of  the  arterial  wall  is  probable.  Now  that  attention  has 
been  directed  to  this  subject,  I  may  say  that  I  think  it 
probable  that  atheroma  may  ultimately  be  found  to  belong 
to  the  enlarging  series  of  affections  having  as  their  immediate 
cause  a  micro-organismal  implantation. 

The  typical  and  classical  changes  present  in  atheroma  are 
seen  in  Figs.  3  and  4. 

In  Figs.  5, 6, and  7,  atheroma  gone  on  to  advanced  calcareous 
infiltration  is  shown,  the  figures  being  taken  from  sections  of 
radial  arteries  which  to  the  finger  were  recognised  as  hard, 
rigid,  and  calcareous  during  life.  In  all  these  arteries  a 
certain  amount  of  fairly  sound  muscular  tissue  has  persisted, 

20 


Fig.  5. — Atheromatous  and  calcareous  radial  artery  (  x  15). 
C,  atheromatous  and  calcareous  ;  C,  media  calcareous ; 
M,  hypertrophied  media  ;   A,  tunica  adventitia. 


Fig.  6. — Calcareous  radial  artery  (  x  15).      C,  the  calcareous 
tunica  intima ;    M,  portions  of  thick  tunica  media. 


OBLITERATIVE  ENDARTERITIS 

while  in  Fig.  5  it  should  be  noted  that  nearly  one-half  of 
the  circumference  of  the  artery  shows,  not  only  an  undegener- 
ate,  but  a  hypertrophied  muscular  coat.  This  anatomical 
fact  is  of  clinical  importance,  as  will  be  shown  in  a  later 
chapter. 

OBLITERATIVE    ENDARTERITIS   AND   ACUTE   AORTITIS. 

The  description  of  obliterative  endarteritis,  as  it  occurs  in 
smaller  arteries,  is  usually  taken  from  the  syphilitic  affection 
found  in  the  brain.  The  affection  there  is  usually  nodular, 
in  the  sense  that  it  affects  a  limited  l^it  of  vessel,  leading  to 
such  thickening  that  a  considerable  node  or  nodule  is  formed. 
The  minute  change  is  a  thickening  of  the  tunica  intima,  the 
thickening  being  the  result  of  a  hyperplasia  of  its  cells. 
It  differs,  however,  from  the  intimal  thickening  in  atheroma 
in  involving  the  intima  somewhat  uniformly,  right  round  the 
vessel,  and  in  showing  no  degeneration.  The  hyperplasia 
which  leads  to  the  thickening  is  progressive,  and  in  its 
progress  encroaches  upon  the  lumen  of  the  vessel,  which  is 
reduced  to  a  minute  size,  or  is  entirely  occluded.  AVhen  an 
artery  is  examined  in  the  acute  stage  a  considerable  amount 
of  small-celled  infiltration  is  present  in  all  three  coats. 
These  changes  in  cerebral  vessels  are  regarded  as  always 
syphilitic.  Corresponding  anatomical  changes  occur  in  the 
arteries  of  the  kidney  in  arterio-sclerotic  atrophy,  and  in 
chronic  interstitial  nephritis ;  they  are  also  met  with  in  the 
lungs  in  fibrosis,  and  m  the  neighbourliood  of  scirrhus 
cancer.  In  these  latter  a  small-celled  infiltration  of  the 
coats  of  the  vessel  does  not  occur,  but  the  thickening  of  the 
intima  goes  on  to  complete  obliteration  of  the  vessel.  A 
corresponding  anatomical  change  also  occurs  in  the  smaller 
nutrient  arteries  in  the  brain.  In  none  of  these — especially  in 
the  lungs,  kidneys,  and  of  course  in  cancer — is  the  change 
regarded  as  of  syphilitic  origin.  I  shall  again  refer  to 
these  changes,  as  they  are  seen  in  the  kidneys,  under  Arterio- 
sclerosis. 

In  the  aorta  an  acute  aortitis  occurs,  giving  rise  to  grey, 
raised,  almost  gelatinous  -  like  areas,  which  on  minute 
examination  show  hyperplastic  thickening  of  the  tunica  intima 

21 


DISEASES  OF  ARTERIES 

and  areas  of  small-celled  infiltration  in  all  three  coats.  This 
condition,  which  anatomically  entirely  corresponds  with  the 
obliterative  endarteritis  of  the  smaller  syphilitic  arteries,  I  hare 
always  regarded  as  of  syphilitic  origin. 

The  condition,  as  it  occm\s  in  the  cerebral  arteries,  is 
represented  in  Fig.  8. 

CALCAREOUS   IXFILTRATIOX    OF    THE    TUNICA  MEDIA. 

Clinically,  calcareous  infiltration  of  the  tunica  media  is 
indistinguishable  from  calcareous  infiltration  of  the  thickened 
intima  in  atheroma.  In  fact,  in  advanced  calcareous  infiltra- 
tion, it  is  by  no  means  always  easy  to  determine  how  much 
of  it  is  intimal  and  how  much  medial.  This  is  owing  to  the 
fact  that  when  it  is  intimal  there  is  so  little  of  the  media 
left  that  the  doubt  arises  whether  it  is  not  the  media  itself 
which  is  infiltrated.  The  position  of  the  elastic  lamina  often 
effectively  helps  in  this  determination.  The  change  is  one 
which  does  not  require  fuller  consideration  here.  In  Figs.  5, 
6,  and  7,  the  media  is  more  or  less  involved  in  the  calcareous 
infiltration. 

ARTERIO-SCLEROSIS. 

In  1901,  in  a  paper  read  before  the  Edinburgh  Medico- 
Chirurgical  Society,  I  submitted  the  results  of  the  examination 
of  the  radial  and  other  arteries,  taken  from  sixteen  cases  which 
had  been  under  my  care,  and  in  which  there  had  been  marked 
thickening  of  the  radial  arteries  during  life.  Since  that  time 
I  have  examined  many  additional  cases,  but  they  have  only 
confirmed  my  previous  observations,  that  the  changes  were 
totally  different  from  those  in  atheroma,  and  strengthened 
the  opinion  I  then  expressed,  that  as  the  term  arterio-sclerosis 
was  in  common  use  it  ought  to  be  retained,  but  its  application 
confined  to  the  changes  which  I  then  showed  to  be  present. 

The  changes  may  be  defined  roughly,  as  great  thickening 
of  the  wall  of  the  artery,  with  diminution  in  the  size  of  its 
lumen. 

The  changes  which  led  to  the  thickening,  when  examined 
in  detail,  were  seen  to  consist  of — (1)  a  marked  thickening  of 


Fig.  7. — Very  calcareous  radial  artery  (  x  15).    Only  a  small  portion 
of  tlie  riglit  and  ujiper  part  of  the  wall  not  involved. 


,\^ 


Fig.  8. — Obliterative  endarteritis  of  syphilitic  origin  (  x  16).     A,  tunica 
adventitia  ;  M,  tunica  media  ;  I,  greatly  thickened  tunica  intima. 


ARTERIO-SCLEROSIS 

the  tunica  media,  clue  to  a  hypertrophy  of  its  muscle  fibres ; 
(2)  a  thickening  of  the  tunica  intima,  clue  to  a  hyperplasia 
of  its  subendothelial  connective  tissue,  without  atheromatous 
degeneration ;  (3)  in  some  instances  fibrous  hyperplasia  and 
thickening  of  the  tunica  aclventitia. 

The  muscular  coat  might  show  some  degeneration,  but 
the  prevalent  notion  that  in  such  thickened  vessels  the 
muscle  of  the  middle  coat  was  replaced  by  fibrous  tissue, 
and  so  the  seat  of  fibroid  degeneration,  was  found  to  be 
entirely  erroneous. 

These  changes  were  not  confined  to  limited  areas  of  vessel 
wall,  as  in  atheroma,  but  affected  uniformly  the  whole  length 
of  the  radial.  They  were  found  to  be  distributed  through- 
out the  body,  the  coronary  and  renal  arteries,  for  instance, 
showing  corresponding  changes.  The  changes  are  shown  in 
Figs.  9,  10,  11,  12,  and  13.  In  Fig.  9  great  thickening  of 
the  artery  is  shown,  and  is  seen  to  be  due  to  hypertrophy  of 
the  tunica  media  and  some  hyperplasia  of  the  tunica  intima. 
Fig.  10,  a  section  of  the  kidney  from  the  same  case,  shows,  in 
the  centre  of  the  field,  an  artery  with  a  much  diminished 
lumen  clue  to  fibrous  hyperplasia  of  the  tunica  intima,  while 
the  tunica  media  is  atrophied ;  at  a  there  is  an  occluded 
arteriole, 

Fig.  11  shows  a  small  thickened  radial  artery,  which  was 
persistently  small  and  hard  during  life.  The  thickening  here 
is  partly  a  hypertonic  contraction,  and  in  part,  I  think,  the 
result  of  a  hyperplasia  of  the  adventitia.  Fig  12,  a  section 
of  the  kidney  from  the  same  case,  shows  two  arteries  with 
their  lumen  encroached  upon  by  hyperplasia  of  the  tunica 
intima,  while  the  tunica  media  is  atrophied.  Fig.  13  is  a 
section  of  the  trunk  of  one  of  the  coronary  arteries,  showing 
hypertrophy  of  the  media  and  hyperplasia  of  the  intima. 
Here,  as  is  sometimes  found,  there  is  also  some  atheromatous 
degeneration  in  the  intima. 

The  changes  were  often  present  when  there  was  practically 
no  atheroma  in  the  aorta  or  the  large  arteries.  They  were, 
however,  sometimes  associated  with  atheroma  of  the  aorta ; 
while  atheroma  of  the  cerebral  arteries  is  so  common  in  later  life, 
that  it,  so  far  as  my  observations  go,  often  accompanies  arterio- 
sclerosis elsewhere. 


DISEASES  OF  ARTERIES 

The  changes  present  in  the  kidneys  are  of  great  interest, 
for  they  seem  to  me  to  explain  the  confusion  which  still 
exists  in  relation  to  vessel  and  kidney  changes  in  "granular 
kidney."  The  changes  in  the  renal  artery  outside  the  kidney 
are  as  I  have  already  described ;  while  the  changes  in  its 
branches  inside  the  kidney  show  a  very  important  modifica- 
tion of,  or  divergence  from,  that  description.  I  found  that, 
inside  the  kidney,  the  arteries  showed  very  marked  fibrous 
hyperplasia  of  their  internal  coat,  going  on  to  complete 
occlusion  of  the  vessel ;  that  the  muscular  coat  as  a  rule 
atrophied  and  might  practically  disappear  as  the  tunica 
intima  thickened ;  and  that  the  external  coat  seemed  to 
become  denser  from  a  proliferation  of  its  fibrous  tissue.  As 
a  result  of  these  changes  the  transverse  section  of  an  artery, 
when  occlusion  was  complete,  showed  like  a  fibrous  globe, 
which  might  be  indistinguishable  from  a  fibroid  glomerulus. 
The  fibrous  tissue  might  be  of  the  hyaline  variety  with  few 
nuclei ;  and  the  change  has  consequently  been  sometimes  re- 
ferred to  as  hyaline  degeneration.  A  corresponding  change 
occurs  in  the  nutrient  arteries  of  the  brain,  and  possibly  in 
other  organs,  which  I  have  not,  however,  examined.  Were 
this  intimal  thickening  compensatory,  in  the  sense  thai 
Thoma  and  his  followers  apply  the  term,  it  would  cease 
with  the  establishment  of  equilibrium.  This,  however,  does 
not  happen,  the  change  going  on  to  vessel  occlusion. 

The  changes  in  the  kidney  vessels  have  been  much 
studied,  and  I  have  given  a  summary  of  the  leading  views 
propounded  on  the  relations  between  the  renal  and  vessel 
changes.  It  appears  to  me  to  be  clear  that  error  arose 
by  applying  the  changes  found  in  the  arteries  inside  the 
kidney  to  all  the  arteries  in  the  body.  The  first  observer 
who  recognised  the  true  nature  of  the  change  in  the  tunica 
media  of  the  systemic  arteries  was  Dr.  George  Johnstone, 
who  named  it  muscular  hypertrophy,  the  reverse  of  the 
condition  which  occurred  in  the  kidney ;  while  Gull  and 
Sutton,  looking  at  the  intimal  changes  and  at  the  kidney 
changes  together,  introduced  the  term  arterio-capillary  fibrosis. 
These  observers  made  the  mistake  of  applying  their  observa- 
tions on  the  kidney  to  the  vessels  generally.  The  result 
was,  that  in  time  the  idea  of  a  diffuse  arterio-capillary  fibrosis 

24 


Fig.  9.—  Showing  great  thickening  of  radial  artery. 


---''    ,S;tv- 


Fig.  10.  — Kidney  from  same  case  as  Fig.  9,  showing,  in  centre  of  field, 
artery  with  greatly  thickened  intima  and  atrophied  media.  At  a,  occluded 
arteriole  (  x  50  diameters). 


CONCLUSION 

so  dominated  the  medical  imagination,  that  the  thick  arteries 
of  chronic  kidney  disease  were,  as  has  abeady  been  mentioned, 
thought  of  as  fibroid,  if  not  as  atheromatous ;  and  if  fibroid 
of  coiu'se  hard  and  rigid !  The  logic  was  sound,  but 
unfortunately  for  truth  the  premises  were  wrong.  To  this 
sound  logic  with  the  faulty  premises  might,  I  think,  be  traced 
not  a  few  of  the  prevailing  misconceptions  regarding 
circulatory  phenomena ;  but,  attractive  as  this  question  is, 
I  do  not  propose  entering  upon  it  here. 

It  is  necessary  to  revert  to  Johnstone's  observations  on 
hypertrophy  of  the  muscular  coat,  for  Savill  in  1897  revived 
this  on  the  strength  of  his  own  observations,  and  called  the 
condition  hyperniyotrophy.  In  a  later  communication  he 
still  more  fully  dealt  with  the  importance  of  the  muscular 
coat  of  arteries ;  but  the  profession  has  shown  no  sign  that 
it  attached  any  practical  significance  to  those  observations 
or  to  the  argument  based  upon  them.  In  Savill's  observa- 
tions there  appears  not  to  have  been  the  thickening  of  the" 
tunica  iutima  which  was  usual  in  my  cases.  In  only  two  of 
my  first  sixteen  cases  was  there  a  pure  hyperniyotrophy 
in  the  radial  artery.  This  point  has  significance,  for  such 
arteries  are  clinically  indistinguishable  from  those  which  have 
the  intima  thickened  also ;  and  as  the  two  conditions  have 
corresponding  causes  I  include  both  under  the  designation  of 
arterio-sclerosis. 

CONCLUSION. 

The  term  Arterio-sclerosis  would  thus  be  applied 
clinically  to  all  thickened  vessels,  other  than  those  thickened 
Ijy  atheromatous  degeneration,  and  would  include — («)  pure 
hypermyotrophy,  (&)  hyperniyotrophy  with  thickening  of  the 
internal  coat,  and  (c)  those  in  which  the  adventitia  was  also 
thickened.  For  clinical  purposes  what  is  required  is  the. 
recognition  of  diffuse  permanent  thickening  which  is  not 
atheroma. 

refeeencp:s. 

Ziegler,  Leltrhuch  cler  Alhj.  Spedellen  Patlioloijischen  Anatomie, 
p.  54.  Thoma,  Vircli.  Arch.,  Bd.  xciii.  and  cxvi. ;  Pathology  and 
Path.  Anatomy,  Eng.  Trans.,  p.  247.     Lancereaux,  Arch.  gen.  de 

25 


DISEASES  OF  ARTERIES 

Med.,  1893,  i.  pp.  5  and  164.  Gueneau  de  Mussy,  Aixh.  gen. 
de  Med.,  1893,  i.  23p-  5  and  164.  Huchard,  Maladies  du  Coeur  et 
des  Vaisseaux,  2 erne  ed.,  Paris,  1893.  Mott,  System  of  Med.,  edited 
by  Clifford  Allbutt.  Osier,  Principles  ajid  Practice  of  Medicine, 
2nd  edition,  p.  700.  George  Johnson,  Med.-Chir.  Transactions,  vols. 
XXX.,  xxxiii.,  xlii.,  li.,  and  Ivi.,  and  Trans.^  Internal.  Med.  Cong., 
1881.  Gull  and  Sutton,  Med.-GJiir.  Transactions,  vol.  Iv. ;  Trans. 
Path.  Sac,  vol.  xxviii. ;  Trans.  Internal.  Med.  Cong.,  1881. 
Dickinson,  Diseases  of  the  Kidney,  1875.  Ewald,  Dreschfeld,  and 
Mahomed,  Discussion,  Trans.  Internat.  Med.  Cong.,  1881.  Samuel 
West,  Granular  Kidney,  1900.  Savill,  Brit.  Med.  Journ.,  Jan.  23, 
1897.  I^othnagel.  Specielle  Pathologie  und  Therapie,  Ed.  xv., 
Erkrankungen  der  Gefasse  L.  v.  Schrotter.  W.  Eussell,  "Arterial 
Hypertonus  and  Arterio-sclerosis ;  their  Eelations  and  Significance," 
Lancet,  June  1,  1901 ;  Transactions,  Medico-Chirurgical  Society, 
Edinhurgh,  vol.  xx.,  1900-1901 ;  Encyclopcedia  Medica,  vol.  xiii.. 
Article,  "Vessels."  Savill,  Trans.  Path.  Soc.  Lond.,  vol.  Iv.,  1904. 
John  M.  Cowan,  Tlie  Practitioner,  Aug.  1905  and  March  1906. 


26 


CHAPTER   IV 
HYPERTONUS  AND  ITS  CLINICAL  RECOGNITION 

(a)  IN   XOX-THICKEXED    AKTEPJES  ; 

(b)  IX    SCLEROSED    AETEPJES  ; 

(c)  IN    ATHEEOMATOUS    AETEEIES. 

HYPERTOXUS   IX   XOX-THICKEXED    AETEEIES. 

A  hypertonic  vessel,  as  has  been  ah'eadj  shown,  is  a  vessel 
the  muscular  coat  of  which  is  unduly  contracted.  As  a  result 
of  the  contraction  its  diameter  is  reduced,  its  wall  is  thicker, 
and  its  lumen  is  smaller.  The  vessel  to  the  finger  feels 
thicker  than  the  perfectly  normal  arterv,  which  is  soft,  thin- 
walled,  and  compressible.  The  degree  of  hardness  varies  of 
course  with  the  amount  of  contraction.  This  increased 
thickness  is  very  commonly  mistaken  for  "  sclerosis "  or 
"atheroma,"  terms  the  significance  of  which  has  been  already 
discussed.  The  thickening  or  hardness  is  commonly  a  uniform 
thickness,  which  can  be  felt  in  the  radial  arteries  as  far  as 
they  can  be  followed  up  the  forearm.  While  this  is  the 
common  character  of  a  hypertonic  artery,  as  revealed  to  the 
sense  of  touch,  it  has  not  always  this  characteristic.  I  have 
frequently  noted  that  an  artery,  which  turns  out  to  Ije  only 
hypertonically  contracted,  may  feel  as  if  it  were  made  up  of 
a  series  of  thickened  rings,  or  plates,  or  segments.  An  artery 
with  these  characters  will  almost  certainly  be  regarded  as 
atheromatous ;  and  it  is  only  by  knowledge  and  experience 
that  one  is  prevented  from  giving  a  premature  opinion,  which 
may  be  totally  wrong.  I  have  observed  these  rings  and 
plates  to  disappear  rapidly  under  treatment  directed  to  relieve 
vessel  contraction.      Thickened  arteries,  especially  if  they  be 

27 


HYPERTONUS  AND  ITS  CLINICAL  RECOGNITION 

considerably  thickened,  as  they  may  be,  liave  come  to  be 
looked  upon  as  having  undergone  permanent  structural 
thickening,  for  which  nothing  can  be  done,  and  which  do  not 
therefore  call  for  further  consideration   from  the  clinician. 

There  is  of  course  no  difficulty  in  determining  when  an 
artery,  such  as  the  radial  or  temporal,  is  thickened  :  the  finger 
trained  "  to  feel  the  pulse  "  has  no  difficulty,  and  there  need 
be  no  dubiety  in  the  mind  of  the  observer  as  to  the  accuracy 
of  his  observations,  for  it  is  as  easy  to  distinguish  between 
degrees  of  thickening  in  arteries  as  it  is  in  rubber  tubes. 
With  a  little  practice,  once  attention  is  drawn  to  the  matter, 
the  smallest  degrees  of  hypertonus  are  recognised  by  the 
increase  in  the  thickness  of  the  wall  of  the  artery.  This 
varying  thickness  has  escaped  ol)servation,  owing  to  so  much 
attention  having  been  given  to  the  consideration  of  blood- 
pressure  or  of  tension. 

Thickened  arteries  are  recognised  by  all  physicians,  and 
are,  as  is  well  known,  of  common  occurrence  ;  the  real  diffi- 
culty arises  in  determining  whether  the  wall  be  thick  from 
hypertonic  contraction,  true  sclerosis,  or  perhaps  even  from 
atheroma.  Atheroma  is  of  relatively  rare  occurrence  in  the 
radial  and  temporal  arteries ;  its  occurrence  is  confined  to 
aged  people,  and  is  usually  associated  with  areas  of  calcareous 
infiltration  which  are  easily  distinguished.  Sclerosis  is,  on 
the  other  hand,  common  after  middle  life.  Before  middle 
life  it  is  fair  to  assume  that  uniform  thickening  is  mainly 
hypertonic,  unless  there  be  discoverable  one  or  otlier  of  the 
two  great  causes  of  early  sclerosis,  namely,  chronic  kidney 
disease  or  syphilis,  to  which  I  think  may  be  added  a  third, 
namely,  the  use  of  malt  and  other  liquors.  The  size  of  the 
vessel  aids  in  the  differentiation  :  an  ordinary  sized  or  a  some- 
what large  vessel  with  a  thick  wall  is  usually  structurally 
thickened ;  a  small  vessel  with  a  relatively  thick  wall  is 
usually  only  hypertonic. 

Fig.  15  was  taken  from  a  section  of  an  artery  which, 
imtil  a  few  days  before  death,  was  soft  and  unthickened. 
Some  days  before  death  it  became  definitely  tightened  up, 
and  the  figure  closely  corresponds  with  the  impression  made 
on  the  finger  before  death  took  place. 

28 


HYPERTONUS  IN  SCLEROSED  VESSELS 

HYPERTONUS   IN   SCLEROSED    VESSELS. 

The  description  of  changes  in  sclerosed  vessels,  given  in 
the  preceding  chapter,  has  prepared  the  way  for  the  acceptance 
of  a  fact  of  great  practical  moment,  namely,  that  sclerosed 
vessels  retain  their  power  of  contractility.  The  significance  of 
the  retention  of  this  movement  has  been  so  under-valued  that 
it  is  hardly  referred  to  in  the  extensive  literature  on  the 
circulation.  It  is  therefore  all  the  more  necessary  to  em- 
phasise the  fact  that  arteries  may  be  the  seat  of  permanent 
structural  thickening,  while  they  are  at  the  same  time 
hypertonically  contracted.  As  has  already  been  stated  in  a 
preceding  section,  the  idea  of  sclerosed  and  atheromatous 
arteries  has  hitherto  carried  with  it  the  idea  of  rigidity. 
This  is  an  unfortunate  association,  for  it  has  led  to  the  idea 
that  thickened  vessels  are  necessarily  permanently  thickened, 
that  they  behave  in  the  body  much  as  rigid  tubes  would 
behave,  and  that  no  remedial  measures  are  available  for  re- 
moving such  anatomical  change.  It  is  true  that  the  structural 
changes  in  sclerosis  are  beyond  therapeutic  influence ;  but 
the  hypertonus  which  frequently  accompanies  it  is  well 
within  the  reach  of  such  influences.  When  these  contentions 
are  accepted,  it  will  be  found  that  the  presence  of  various 
symptoms  lead  to  the  diagnosis  of  the  hypertonic  factor  in 
sclerosed  vessels  and  to  its  appropriate  treatment. 

Sclerosed  vessels  not  only  retain  some  measure  of  con- 
tractility, but  it  has  seemed  to  me  that  they  are  abnormally 
responsive  to  some  at  least  of  the  influences  which  determine 
arterial  contraction.  This  seems  to  be  the  case  particularly 
in  old  people.  There  is  evidently  a  possible  fallacy  here, 
for  in  old  people  the  eliminative  processes  are  so  impaired 
that  the  apparent  increase  of  sensitiveness  may  be  regarded, 
perhaps  more  properly,  from  this  standpoint ;  the  quick 
muscular  response  only  indicating  a  more  ready  saturation  of 
the  blood  with  such  waste  substances  as  act  on  the  vessels, 
the  response  really  remaining  normal.  For  practical  pur- 
poses, it  is  however  of  great  importance  to  know  that 
there  is  in  most  aged  people  this  quick  and  ready  re- 
sponse, and,  when  a  measure  of  confidence  is  acquired 
in     recognising     hypertonic    contraction,    any    dubiety    that 

29 


HYPERTONUS  AND  ITS  CLINICAL  RECOGNITION 

may  exist  as  to'  the  probability   of  such  a  sensitiveness  will 
be  lost. 


HYPERTONUS   AND   RELAXATION   IN   ATHEROMATOUS 
ARTERIES. 

As  has  been  indicated  in  an  earlier  chapter  the  common 
conception  of  a  sclerosed  artery  is  that  it  is  a  rigid  tube.  This 
conception,  as  we  have  shown,  was,  borrowed  from  the  teaching 
resardino;  the  vessels  in  advanced  atheroma,  and  it  is  in 
accordance  with  experience  that  the  extreme  example  be- 
comes the  standard  type.  This  common  conception  is,  how- 
ever, erroneous,  and  seriously  misleading.  It  is  only  in 
atheroma  with  much  calcareous  infiltration  that  the  artery 
becomes  practically  a  rigid  tube.  In  my  study  of  the  arterial 
wall  I  have  frequently  been  surprised  to  find  the  amount  of 
relaxation  that  took  place  in  a  vessel  that  was  clearly  the 
seat  of  much  calcareous  infiltration.  In  other  cases  where, 
from  the  hooped  and  segmented  character  of  the  thickenings, 
there  seemed  little  doubt  that  the  thickenings  were 
atheromatous,  they  could  no  longer  be  felt  when  the  vessel 
became  relaxed.  In  this  latter  class  of  case  the  character  of 
the  artery  to  the  sense  of  touch  is  probably  due  to  irregular 
thickenings  of  the  intima  plus  hypertonic  contraction,  the 
thickenings  not  being  felt  when  the  w^all  becomes  soft,  by  the 
passing  oft'  of  the  hypertonus,  or  it  may  be  due  merely  to 
irregularity  in  the  muscular  coat  itself.  In  other  cases  the 
rigid  segments  persist,  no  matter  what  measures  be  taken  for 
the  removal  of  the  hypertonic  contraction ;  and  yet  in  a 
considerable  number  of  such  cases  it  is  quite  plain  to  the 
finger  that  a  measure  of  relaxation  can  be  eft'ected.  That 
relaxation  under  such  conditions  occurs  is  due  to  the 
anatomical  fact,  that  in  atheroma  it  is  rare  for  the  entire 
circumference  of  the  vessel  to  be  aft'ected ;  there  is  usually  a 
considerable  part  of  it  where  there  is  only  moderate  thicken- 
ing of  the  tunica  intima ;  and  where  the  muscular  coat  can 
relax  and  contract  so  as  to -appreciably  affect  the  condition  of 
the  wall.  The  idea  of  the  fixed  and  rigid  tube  has  to  be 
given  up,  save  in  extreme  cases.  That  the  recognition  of 
such  arterial   changes  is  not   due  to  a  personal  delicacy   of 

30 


RELAXATION  IN  ATHEROMATOUS  ARTERIES 

touch  is  proved  by  the  fact  that  my  hospital  assistants  and 
others,  with  whom  I  am  brought  into  close  association,  readily 
acquire  the  skill,  once  their  attention  has  been  directed 
to  individual  cases  and  the  significance  of  the  phenomena 
explained  to  them. 

The  condition  of  the  arterial  wall  in  advanced  atheroma 
with  calcareous  infiltration  has  been  shown  in  Figs.  5,6,  and  7. 
Fig.  7  was  taken  from  a  patient  with  very  stiff  vessels, 
and  yet  I  had  no  doubt  that  these  vessels  tightened  up  a 
little  and  relaxed  a  little  under  treatment. 

I  may  here  refer  to  two  cases  illustrating  this  point,  which 
made  a  special  impression  upon  me,  from  certain  associations. 

The  first  case,  Mrs.  M.,  aged  49,  a  patient  wdio,  simul- 
taneously with  attacks  of  angina  pectoris,  developed  motor 
paresis,  had  a  radial  artery  which  felt  as  if  composed  of 
hard  segments,  which  were  regarded  as  atheromatous,  and  yet 
this  character  entirely  disappeared,  the  wall  becoming  uni- 
formly soft,  under  treatment  which  led  to  relaxation  of  the 
arterial  wall.  Whenever  the  vessel  tightened  up,  it  showed 
the  same  irregular  thickening.  This  case  is  given  in  greater 
detail  at  p.  176. 

Case  1,  an  Irishman,  aged  56,  was  admitted  to  Ward  3, 
for  alcoholism.  On  admission,  he  was  so  restless  and 
tremulous,  that  it  was  impossible  to  get  an  absolute  record  of 
his  arterial  pressure;  it  seemed  to  be  considerably  above  200. 
He  soon  quieted  down,  and  he  acknowledged  that  he  had 
been  drinking  too  much  all  his  life,  while  for  the  last  fifteen 
months  his  drinking  was  only  limited  by  monetary  barriers. 
He  drank  whisky  and  rum,  and  was  amused  at  the  suggestion 
that  he  had  a  preference  for  either,  seeing  he  was  so  apprecia- 
tive of  each.  His  right  radial  artery  was  thick  and  hard  and 
marked  by  rigid  segments,  such  a  vessel  as  my  clinical 
assistant  spoke  of  as  feeling  so  brittle  that  it  gave  one  the 
idea  that  it  would  crack  if  it  were  fingered  roughly.  The 
pressure  was  190.  Under  erythrol  first,  and  then  under 
iodide  of  potassium  and  squill,  the  vessel  became  larger 
and  softer,  and  although  the  thickened  segments  were  still 
perceptible  they  were  not  nearly  so  rigid,  and  the  vessel  lost 
that  character  which  gave  to  it  at  first  its  brittle  feel.  Along 
with  this  change  in  the  character  of  the  vessel,  the  pressure 

31 


HYPERTONUS  AND  ITS  CLINICAL  RECOGNITION 

fell  to  170.  No  one  who  followed  the  changes  in  this 
man's  radial  artery  would  have  had  any  difficulty  in  being 
convinced  of  the  accuracy  of  these  statements.  The  effect  on 
the  vessel  was  produced  hj  physical  rest  in  bed  and 
abstinence  from  alcohol,  but  mainly  by  the  action  of  the 
druo;s  administered. 


CHAPTER   V 
THE  CAUSES  OE  HYPERTONIC  CONTRACTION 

1.  INFLUENCE    OF    THE    NEKA^OUS    SYSTEM. 

2.  INFLUENCE  OF  THE  COMPOSITION  OE  CONDITION  OF  THE 
BLOOD. 

3.  THE  LOCALISATION  OF  THE  ACTION  ON  THE  VESSEL 
WALL. 

4.  INFLUENCE    OF    TOBACCO. 

Having  dealt  with  hypertonic  contraction  as  it  occurs  in 
normal,  in  sclerosed,  and  in  atheromatous  arteries,  we  next 
proceed  to  consider  the  causes  which  determine  this  move- 
ment on  the  part  of  the  arteries.  Let  me  again  repeat  that 
this  property  separates  the  arteries  altogether  from  the 
vulgar  mechanical  conception  which  would  make  them  mere 
elastic  tubes. 

With  regard  to  hypertonic  contraction,  the  general 
]3roposition  may  be  submitted,  that  it  is  caused  by  one  or 
other  of  two  factors  : 

First — The  intluence  of  the  nervous  system. 

Second — The  composition  or  condition  of  the  blood. 

The  converse  of  hypertonus  is  either  a  relaxation  -of 
hypertonus  or  a  diminution  in  normal  or  average  tone. 

We  may  now  consider,  in  some  detail,  the  positive  aspect 
of  this  subject,  which  is  the  more  important,  while  not  for- 
getting that  the  negative  has  an  importance  of  its  own. 

THE    INFLUENCE    OF   THE    NERVOUS    SYSTEM. 

Taking  up  first  the  influence  of  the  nervous  system,  it  is 
universally  known  that  the   relations  of    the  blood-vascular 
C  33 


THE  CAUSES  OF  HYPERTONIC  CONTRACTION 

system  to  the  nervous  system  have  been  traced  and  deter- 
mined by  long  and  careful  experimental  investigation. 

The  investigation  of  these  relations  has  been  so  detailed, 
and  the  results  have  been  so  striking,  that  teachers,  and 
through  them  students  and  practitioners,  have  almost  come  to 
regard  the  vessels  as  the  toy  of  the  nervous  system, — that 
their  manifestations  merely  mirror  nervous  influences. 
The  effect  of  various  emotions  upon  them  was  too  apparent 
and  too  assertive  to  escape  observation,  or  not  to  demand 
recognition.  The  path  by  which  emotion  travelled  was  traced, 
and  the  controlling  power  of  the  vasomotor  centre  in  the 
medulla  was  determined.  The  result  has  been  that  the  vaso- 
motor mechanism  thus  revealed  has  appealed  so  strongly  to 
the  medical  imagination  that  the  play  or  movement  of  the 
arteries  has  been  thought  of  through  the  nervous  system  only : 
as  if  they  had  no  identity,  as  if  they  were  the  mere  weather- 
cocks of  every  gust  of  nervous  influence,  the  bond-slave  of  the 
higher  system.  The  nervous  side  of  the  vasomotor  mechanism 
has  been  regarded  as  supreme ;  as  instigating,  regulating, 
controlling,  and  determining  all  vascular  phenomena,  even 
those  attendant  upon  the  activities  and  exhaustions  of  organs 
and  tissues.  The  names  of  Claude  Bernard,  Brown- Sequard, 
Waller,  and  Schiff  are  "  household  names "  in  this  con- 
nection. I  need  not  dwell  at  length  on  the  achievements 
of  physiological  investigation  in  this  department ;  they 
are  well  known,  and  I  have  indicated  that  they  have  not 
hitherto  been  underrated.  Their  very  brilliance  has,  I 
venture  to  think,  seriously  blinded  us  to  the  fact  that 
physiological  investigation  has  also  shown  that  there  is 
another  factor  which  influences  and  determines  the  move- 
ment or  play  of  the  vessel  wall ;  that  factor  being  the 
composition  of  the  circulating  fluid  itself.  It  is  with  this 
factor  that  I  mainly  deal  in  these  pages,  and  I  hope  to  show 
that  the  failure  to  appreciate  aright  this  aspect  of  the 
circulation  has  prevented  our  understanding  many  things ; 
while  its  recognition  makes  many  things  clear.  I  hope  to 
show  that  the  prevalent  view  is  too  exclusive,  is  incomplete, 
and  correspondingly  inaccurate  and  misleading. 


34 


INFLUENCE  OF  THE  COMPOSITION  OF  THE  BLOOD 

THE    IXFLUEXCE    OF    THE    COMPOSITION   OF    THE  BLOOD 

It  has  l^een  long  known  that  a  number  of  substances  used 
therapeutically  act  directly  upon  the  vessel  wall, — that  is, 
without  the  medium  of  the  nervous  mechanism,  leading  to 
contraction  or  relaxation  of  its  muscular  coat.  Blake  claims 
to  have  been  the  first  to  show  that  by  injecting  infusion  of 
digitalis  into  the  arteries  contraction  resulted.  This  observa- 
tion was  made  as  long  ago  as  1839.  Einger  and  Sainsbury's 
investigations  are  more  recent,  are  widely  known,  and  may 
indeed  be  regarded  as  having  determined  the  views  regarding 
the  action  of  digitalis  which  we  all  hold.  Their  experimental 
investigations  confirmed  Blake's  observation  ;  liut  they  further 
showed  that  digitalis  acted  independently  of  the  nervous 
mechanism,  acting  directly  upon  the  vessel  wall.  This  was 
shown  by  isolating  the  vessels  from  their  nerve  supply. 

Donaldson  and  Stevens,  experimenting  with  digitaliu, 
foimd  that  it  caused  constriction  of  the  arterioles,  probably 
through  its  action  on  the  muscular  coat.  They  further 
showed  that  it  acted  on  the  capillaries  as  well  as  the 
arterioles. 

Haynes,  investigating  the  action  of  the  digitalis  group 
upon  the  heart,  noted  that  although  the  coronary  arteries  are 
not  innervated  (sic),  squill  and  digitahs  cause  some  constriction 
of  them,  probably  by  irritant  action. 

Dale,  investigating  the  mode  of  action  of  ergot,  has 
shown  that  the  primary  or  stimulant  action  of  this  substance 
is  a  vaso-constrictor  action,  which  is  quite  independent  of 
the  vasomotor  centre.  This  investigation  I  shall  have  again 
to  refer  to. 

Experiment  has  further  shown  that  if  blood  be  mixed 
with  aniyl  -  nitrite,  chloral  hydrate,  morphine,  quinine,  or 
atropine,  and  made  to  pass  through  the  vessels  of  a  recently 
excised  organ,  dilatation  of  its  vessels  takes  place  :  digitaliu 
and  veratrin  used  in  the  same  way  cause  contraction. 

Professor  Halliburton,  experimenting  with  choline,  pro- 
duced by  its  means  a  temporary  fall  in  arterial  pressui'e, 
due  in  part  to  its  action  on  the  heart,  Ijut  mainly  to  dilata- 
tion of  peripheral  vessels,  especially  in  the  intestinal  area. 
The  action  is   due,  he   shows,   to    the   direct  action    of    this 

35 


THE  CAUSES  OF  HYPERTONIC  CONTRACTION 

sulistance  ou  the  neuro -muscular  apparatus  of  the  vessels, 
the  same  effect  being  produced  after  the  influence  of  the 
central  nervous  system  was  removed.  Xeurine,  on  the 
other  hand,  causes  peripheral  constriction. 

From  these  alone  it  would  seem  as  if  Professor  Leonard 
Hill  were  over-cautious  in  saying  that  "  it  is  conceivable 
that  the  quality  as  well  as  the  tension  of  the  blood  may  be 
the  exciting  cause  of  vascular  tone."  It  is  quite  clear  that 
there  is  sufficient  evidence  to  prove  that  the  arterial  and 
capillary  walls  can  be  stimulated  to  contract  by  the  presence  of 
substances  in  the  blood  acting  directly  upon  them.  Therefore 
the  composition  of  the  blood  is  more  than  "  conceivably  "  a 
factor  in  maintaining,  influencing,  increasing  or  diminishing 
vessel  tone. 

If  we  turn  from  the  experimental  side  and  inquire 
regarding  the  views  held  ou  the  clinical  side,  it  will  be 
found  that  there  is  a  great  mass  of  belief  that  substances 
present  in  the  blood  affect  blood-pressure. 

Dr.  Broadbent,  later  known  as  Sir  William  Broadbent, 
in  his  masterly  little  book  on  The  Pulse  gives  capillary 
resistance  as  a  cause  of  high  tension,  holds  that  certain 
substances  in  small  quantities  cause  resistance,  and  mentions 
digitalis,  ergot,  carbonic  acid,  nitrogenous  waste,  and  the 
products  of  imperfect  metabolism  as  examples  of  such 
action.  Broadbent,  of  course,  knew  that  some  at  least  of 
the  substances  enumerated  caused  contraction  of  arterioles 
and  capillaries,  and  yet  his  words  suggest  to  me  that  he 
thought  of  modifications  in  the  composition  of  the  blood  as 
causing  difficulty  in  its  passage  through  the  capillaries 
rather  than  of  the  difficulty  being  caused  by  capillary  or 
arteriole  contraction.  The  conception  of  altered  composition, 
of  something  added  to  the  Idood,  rendering  its  flow  more 
difficult  through  the  peripheral  vessels,  is  practically  the 
same  view  as  is  expressed  in  the  term  "  increased  viscosity," 
the  view  towards  which  Professor  Clifford  Allbutt  definitely 
leans,  wdiile  his  philosophic  mind  and  wide  practical  experi- 
ence do  not  allow  him  to  wholly  adopt  it. 

However  attractive  the  idea  of  increased  viscosity  may 
be,  it  is  necessary  to  realise  that  there  is  no  convincing 
evidence  that  deleterious  substances,  such  as  clinically  may 

^.6 


INFLUENCE  OF  THE  COMPOSITION  OF  THE  BLOOD 

be  assumed  to  l^e  present  in  the  blood,  so  affect  its  \dscosity 
or  specific  gravity  as  to  impede  its  flow  through  the 
arterioles  and  capillaries.  In  cholera  certainly,  and  probably 
in  other  conditions  with  great  intestinal  flux,  the  blood 
becomes  so  inspissated  as  to  seriously  impede  its  flow :  but 
in  such  a  condition  as  chronic  interstitial  nephritis,  that 
there  should  be  anything  approaching  this  state  is  a  very 
different  matter.  With  a  free  supply  of  fluid  it  is  difficult 
to  think  of  the  viscosity  of  the  blood,  thereby  meaning  its 
specific  gravity,  being  seriously  modified,  seeing  that  fluid 
is  so  readily  taken  up  and  discharged  from  it. 

Huchard  holds  that  excess,  and  above  all  errors,  in 
alimentation,  throw  toxic  substances  into  the  blood  which 
produce  a  state  of  spasm  of  the  arterial  system,  followed  by 
hyper-tension  and  arterio-sclerosis. 

Senator  and  many  others  hold  corresponding  views 
with  regard  to  the  importance  of  the  presence  of  nitro- 
genous waste  products  in  the  blood. 

The  general  conception  undoubtedly  is  that  "  nitrogenous 
waste,  and  the  products  of  imperfect  metabolism,"  to  repeat 
Broadbent's  words,  when  present  in  the  blood,  raise  blood- 
pressure.  It  is  not  necessary  to  elal^orate  this  point 
further ;  the  literature  of  kidney  disease,  and  more  recently 
of  blood-pressure,  is  full  of  it,  not  to  go  further  afield  for 
examples.  The  explanation  of  the  raised  blood-pressure  has 
usually  been  referred  to  increased  peripheral  resistance,  and 
there  the  matter  has  as  a  rule  been  left ;  although,  as  has 
been  said,  critical  and  accomplished  physicians  hke  Broadbent 
and  Allbutt  have  seen  that  this  term  in  the  ecjuation 
wants  determining,  while  to  others  the  phrase  in  itself 
has  been  all-satisfying. 

My  contention  is  that  certain  suljstances  present  in 
the  blood,  even  in  small  cj^uantity,  cause  arterial  and 
capillary  contraction.  This  is  the  fundamental  fact,  and 
will  be  found  to  be  the  first  step  in  all  raising  of  blood- 
pressure  which  goes  on  to  arterio-sclerosis.  Even  a  slight 
degree  of  such  contraction  means  peripheral  resistance. 
There  is  indeed  no  need  to  go  beyond  vascular  contraction 
for  the  explanation  of  peripheral  resistance ;  it  is  the 
simj)lest  explanation,  as   it  is  the  most  certain  factor,  and, 

37 


THE  CAUSES  OF  HYPERTONIC  CONTRACTION 

be  it  remembered,  not  necessarily  brought  about  through  the 
nervous  system. 

As  the  capillaries  contract  as  well  as  the  arteries,  the 
"  stop-cock "  theory  of  Dr.  George  Johnstone  must  yield  to 
the  more  prosaic  view  that  arteriole  contraction  is  but  part 
of  a  wider  contraction,  and  is  not  a  special  arrangement  for 
saving  the  capillaries.  If  we  are  to  retain  any  part  of  this 
attractive  conception,  it  will  require  to  be  so  modified  that 
arteriole  and  capillary  contraction  may  be  regarded  as  a 
provision  for  diminishing  the  supply  of  an  impure  blood 
to  the  tissues.  This  is  really  a  truer  conception,  for  it  is 
the  good  of  the  tissues  which  is  the  aim  of  the  circulation, 
and  this  vessel  constriction  not  only  protects  directly,  but 
also  indirectly,  by  producing  symptoms  which  can  lead  to 
what  we  may  call  blood  purification. 

The  mechanical  views  of  the  circulation  have  had  their 
day,  and  have  effected  their  purpose  almost  too  well ;  it  is 
now  time  that  we  should  think  of  the  vessels  as  living  tubes, 
contracting  not  only  under  the  influence  of  nerve  centres, 
but  under  the  direct  stimulus  of  substances  present  in  the 
circulating  blood — contraction  so  caused  being  the  liypcr- 
tonus  and  the  hypertonic  contraction  of  our  argument  as 
much  as  when  it  is  a  response  to  nerve  impulses. 

THE    LOCALISATION    OF   THE   ACTION   ON   THE   VESSEL 

WALL 

The  fact  that  arterial  contraction  can  Ije  determined  by 
blood  composition,  or  by  l^lood-content,  has,  as  has  been 
already  said,  but  little  influenced  practical  medicine.  It  is 
therefore  all  the  more  necessary  not  only  to  show,  as  I  have 
just  done,  that  the  proposition  is  supported  by  the  weight  of 
physiological  investigation,  as  surely  as  the  action  of  the 
sympathetic  nervous  system  is  established,  but  to  see  how 
much  further  physiological  investigation  and  experiment 
will  allow  us  to  go. 

It  will  be  seen  that  experimental  investigations  still 
further  warrant  and  support  our  clinical  contentions ;  and 
they  ought,  I  think,  to  satisfy  and  convince  those  who 
have    hitherto   thouQ-ht  of  vessel    contraction    and    of    blood- 


LOCALISATION  OF  ACTION  ON  VESSEL  AVALL 

pressure  only  or  mainly  from  the  side  of  the  vasomotor 
nervous  mechanism. 

The  point  which  I  think  it  is  so  desirable  to  consider  is 
what  Elliott  speaks  of  as  "  the  localisation  of  the  action  "  of 
the  substances  which  have  been  experimented  with ;  that 
is,  the  particular  element  or  part  of  the  vessel  wall  which, 
when  stimulated,  leads  to  contraction,  although  the  vaso- 
motor nerve  connections  are  severed. 

The  point  has  been  investigated  by  means  of  adrenalin, 
the  action  of  which  as  a  vaso-constrictor  is  well  known.  The 
work  of  Oliver  and  Schafer,  Langley  and  others  in  this  country, 
of  Cybulski,  Boruttau  and  others  on  the  continent,  have  fully 
established  the  possession  of  this  remarkable  action  on  the 
part  of  this  substance  as  obtained  from  the  suprarenal  glands. 

Lewandowsky,  investigating  the  action  of  adrenalin,  sug- 
gested that  its  action  on  plain  (unstriped)  muscle  simulated 
that  which  follows  on  electrical  stimulation  of  the  sympathetic 
nerves  supplying  the  special  part  being  examined.  Langley 
followed  this  up,  and  showed  that  the  extent  of  contraction 
of  the  blood  vessels  in  the  various  organs  varied  with  their 
control  by  vasomotor  nerves. 

ElKott  has  still  further  sustained  and  elaborated  the 
preceding  investigations.  The  conclusion  at  which  he 
arrives  is  as  follows :  "  The  reaction  to  adrenahn  of  any 
plain  muscle  in  the  body  is  of  a  similar  character  to  that 
following  excitation  of  the  sympathetic  (thoracico-lumbar 
visceral,  or  autonomic)  nerves  supplying  that  muscle,  and 
the  extent  of  the  reaction  varies  directly  with  the  frequency 
of  normal  physiological  impulses  received  by  the  muscles  in 
life  through  the  sympathetic  nerves."  As  regards  the 
action  on  the  blood  vessels,  he  says  that  "  the  parallel 
action  of  the  sympathetic  nerves  and  of  adrenalin  is  main- 
tained in  the  heart  and  blood  vessels."  This  constriction 
is  produced  in  the  largest  arteries  as  well  as  in  the  arterioles. 
It  is  not  evident  in  the  veins.  Erom  Exner  and  Melzer's 
experiments  by  intraperitoneal  injection  it  seems  more  than 
probable  that  the  capillaries,  at  least  in  certain  regions  of 
the  body,  are  also  constricted  by  adrenalin. 

The  fact  of  constriction  being  thus  established,  the 
question   necessarily   arises,  does   the  adrenalin  act    through 

39 


THE  CAUSES  OF  HYPERTONIC  CONTRACTION 

the  vasomotor  nervous  mechanism  or  upon  the  vessel  wall  ? 
These,  as  in  the  case  of  the  heart,  may  be  regarded  respect- 
ively as  the  neurogenic  and  the  myogenic  views.  That  the 
stimulation  is  produced  at  the  periphery  was  proved  by 
Brodie  and  Dixon,  who  found  that  the  vaso-constrictor  nerves 
to  the  limbs  lost  their  electrical  irritability  within  three 
hours  of  death,  while  the  vessels  reacted  to  adrenalin  six 
hours  after  death.  Degeneration  of  the  sympathetic  nerves 
after  section  does  not  hinder  the  action  of  adrenalin  upon 
the  vessels.  These  investigators  located  the  point  of 
stimulation  in  the  "  connecting  link  between  nerve  fibre  and 
muscle  fibre,  .  .  .  which  is  not  necessarily  a  constituent 
part  of  the  muscle  fibre,  nor  yet  of  the  nerve  fibre,"  and 
they  designate  it  "  neuro-muscular  junctional  tissue." 

Elliott's  comment  on  this  is  that  "  when  plain  muscle 
develops  connection  with  sympathetic  nerves,  it  must  at  the 
myoneural  junction  acquire  a  mechanism  that  can  receive  the 
nervous  impulse  "  ;  further,  "  adrenalin  excites  not  the  muscle 
fibre  directly,  but  a  substance  developed  out  of  it."  He 
repeats  and  amplifies  this  as  follows :  "  The  irritability  of 
the  muscle  toward  adrenalin  depends  on  the  differentiation 
of  part  of  its  substance  to  form  the  myoneural  junction. 
And  it  has  been  shown  that  the  sensitiveness  of  reaction 
depends  on  the  frequency  with  which  it  receives  sympathetic 
nervous  impulses  in  the  reflexes  of  daily  life.  Once,  however, 
the  sensitiveness  has  been  developed,  it  does  not  in  the  life 
of  the  individual  become  dulled  by  the  total  abeyance  of 
arriving  impulses,  such  as,  for  instance,  is  caused  by  degen- 
erative section  of  the  nerves.  Then,  indeed,  the  junction 
acquires  an  exaggerated  irritability." 

This,  however,  does  not  exhaust  the  interest  of  this  subject. 
Another  experimenter,  Mr.  H.  H.  Dale,  in  a  most  important 
study  of  the  action  of  ergot,  has  shown  that  its  primary  action 
upon  the  circulatory  system  is  stimulant, — that  is  to  say,  that 
it  leads  to  contraction  of  the  vessel  w^all,  this  being  the  well- 
known  vaso-constrictor  action  which  has  led  to  its  use  as  a 
therapeutic  agent  in  practice.  This  vaso-constriction  leads,  of 
course,  to  a  rise  of  blood-pressure  in  the  aorta,  and  is  held  by 
this  observer  to  be  quite  independent  of  the  vasomotor  centre. 

Although  the  vaso-constrictor  action  of  ergot  is  as  widely 

40 


LOCALISATION  OF  ACTION  ON  VESSEL  WALL 

known  as  anv  fact  in  medicine,  it  is  certainly  not  equally 
known  that  there  is  a  further  action,  brought  about  bv  larger 
doses,  which  is  its  secondary  or  paralytic  action.  That  is  to 
say,  large  doses  of  ergot  lead  to  dilatation  of  vessels  instead 
of  to  constriction.  When  ergot  has  been  used  in  sufficient 
quantity  to  produce  this  effect  upon  the  vessel  the  vessel  no 
longer  responds  to  the  application  of  adrenalin :  that  is,  adrenalin 
can  no  longer  constrict  it.  The  action  of  the  ergot  is  to 
paralyse  the  myoneural  junctions  on  which,  as  has  been  already 
shown,  adrenalin  acts.  With  the  paralysis  of  the  junctions  the 
constrictor  effect  of  stimulating  the  sympathetic  is  also  lost. 

There  is  another  gland  in  the  body,  which,  as  Ohver  and 
Schiifer  have  shown,  produces  a  substance  which  has  a  like 
vaso-constrictor  action  to  adrenalin — the  gland  being  the 
Pituitary  Body,  or  rather  its  infundibular  portion.  The  con- 
strictor or  pressor  principle  in  this  gland  produces  its  stimulant 
effect  directly  on  the  arterial  wall,  not  on  the  vasomotor 
nervous  mechanism.  Yet  the  remarkable  fact  has  been 
chsclosed  by  Dale,  that  ergot  in  large  quantity  does  not 
neutralise  its  action,  as  it  neutralises  the  action  of  adrenalin. 
Dale  says  that  the  constrictor  or  "  pressor  principle  contained 
m  pituitary  extracts  produces  its  stimulant  effect  on  the 
arterial  muscle,  not  through  any  part  of  the  sympathetic 
nervous  apparatus,  not  through  the  related  structures  on 
which  adrenalin  acts,  but  through  some  other  substance 
or  substances  of  the  muscle  fibres  themselves." 

It  is  therefore  plain  and  evident  that  vessels  constrict  by 
the  direct  influence  of  substances  in  the  blood.  The  conception 
which  has  so  long  dominated  our  views,  and  it  is  hardly  too 
much  to  say  sealed  our  eyes,  that  vessel  contraction  or 
relaxation,  or  the  associated  alterations  in  blood-pressure,  are 
the  manifestations  of  nervous  impulses,  has  to  be  given  up  in 
great  part,  and  must  share  its  honours  with  tlie  other  factor. 

While  the  direct  influence  of  constrictor  substances  on  the 
vessel  wall  is  thus  established,  it  is  to  be  noted  how  subtle 
the  processes  are :  adrenalin  acts  upon  what  is  neither  nerve 
nor  muscle,  but  is  euphoniously  termed  the  myoneural  junction  : 
pituitary  extract  acts  on  the  vessel  wall  as  adrenalin  does,  not, 
however,  upon  nerve,  nor  upon  the  myoneural  jmiction,  but  upon 
some  substance  which,  as  it  is  none   of  the   things  mentioned, 

41 


INFLUENCE  OF  TOBACCO 

is  assumed  to  be  muscular.      Choline  acts  in  the  same  way, 
but  its  action  can  be  prevented  or  neutralised  by  atropine. 

How  futile  seem  the  controversies  regarding  the  neuro- 
genic or  myogenic  origin  of  vascular  response  !  How  many 
controversies  have  been  waged  over  alternatives,  when  each 
was  but  part  of  a  more  central  truth  ! 

THE   INFLUENCE    OF    TOBACCO 

In  Chapter  XV.,  which  deals  with  angina  pectoris,  it  is 
pointed  out  that  one  of  the  recognised  clinical  varieties  of  the 
affection  is  the  toxic  form.  I  illustrate  this  form  by  reference 
to  the  effect  an  overdose  of  tobacco  may  have  on  myself. 
The  cardiac  discomfort  accompanying  the  hypertonic  con- 
traction noticed  in  the  radial  artery  illustrates  what  is  perhaps 
the  mildest  form  of  angina  pectoris  that  can  be  experienced. 
It  is,  however,  difficult  to  determine  through  which  system 
tobacco  acts,  so  I  give  it  this  special  paragraph  here.  Tobacco 
is  much  used,  and  its  influence  upon  the  vessels  has  definitely 
attracted  the  attention  of  clinicians.  Personally  I  have  not 
so  far  paid  any  special  attention  to  it,  but  my  clinical 
assistant.  Dr.  J.  L.  Green,  has  recently  made  observations  on 
himself  and  a  friend.  He  tells  me  that  if  he  or  his  friend 
inhales  a  cigarette  made  of  Virginian  tobacco,  the  hypertonic 
contraction  of  the  radial  artery  which  ensues  is  very  marked, 
and  that  with  the  liardening  of  the  vessel  the  heemomauometer 
reading  rises  15  mm.  Hg.  Here,  as  in  other  instances,  the 
fact  is  the  constriction  of  vessels.  What  the  blood-pressure 
may  be  inside  the  constricted  vessels  is  a  proUem  dealt  with 
in  other  chapters. 

REFERENCES. 

Halliburton,  Biucliemistry  of  Muscle  and  Nerve,  1904,  p.  119 
et  seq.  H.  H.  Dale,  Journ.  of  Physiol.,  vol.  xxiv.  No.  3. 
Donaldson  and  Stevens,  Journ.  of  Physiol.,  1881,  vol.  iv.  Landois, 
Physiology,  10th  ed.,  1904.  Broadbent,  The  Pulse.  Leonard  Hill, 
Schafer's  Phystoloriy.  Elliott,  Journ.  of  Physiol.,  1905,  vol.  xxxii. 
p.  401.  Senator,  Folia  Therapeutica,  A])n\  1907,  p.  37.  Oliver  and 
Schafer,  Journ.  of  Physiol,  vol.  xviii.,  1895,  pp.  230  and  277. 
Schafer  and  Vincent,  ibid.,  vol.  xxiv.  p.  xix.  1899.  Brodie  and  Dixon, 
ihicl.,  vol.  XXX.,  1904,  p.  494.  Langley,  ihid.,  vol.  xxxiii.,  190.5-6, 
p.  374.  LeAA^andowsky,  Arch,,  f.  Anat.  u.  Physiol.,  1899,  p.  360. 
Ringer  and  Sainsbury,  Med.  Chi.  Trans.,  vol.  Ixvii.  Haynes,  Bio- 
Chemiccd  Journ.  vol.  i.,  Feb.  1906. 

42 


CHAPTER   VI 

THE  CLINICAL  ESTIMATION  OF 
BLOOD-PRESSURE 

1.  AETEEIAL    TENSIOX    AND    BLOOD-PKESSUEE. 

2.  METHODS    OF    ESTIMATING    BLOOD-PEESSUEE. 

3.  THE  FAGTOES  WHICH  DETEEMINE  H^MOMANOMETEE  EEADINGS. 

ARTERIAL   TENSION   AND    BLOOD-PRESSURE. 

Foe  many  years  the  attention  of  clinicians  has  been  largely 
directed  to  what  has  been  called  "  arterial  tension."  The 
significance  to  be  attached  to  the  term  has  been  variously 
interpreted ;  its  relation  to  blood-pressure  has  been  dis- 
cussed by  Professor  Clifford  Allbutt  and  others.  In  its 
everyday  and  ordinary  use  there  is  no  doubt  it  has  been 
associated  with  much  confusion  of  idea  and  serious  error. 
Allbutt,  with  his  critical  faculty,  decides  that  the  word 
"  tension "  is  practically  not  applicable  to  the  blood  inside 
the  vessel,  and  with  this  I  entirely  agree.  If  it  is  not  to 
be  referred  to  the  l_ilood,  it  might  be  assumed  that  it  is 
applicable  to  the  vessel  wall.  It  is  not,  however,  proposed 
to  attempt  to  discuss  the  various  shades  of  meaning  the  word 
"  tension  "  may  have, — that  may  Ije  left  to  the  pundits  in 
physics.  And  yet  I  cannot  leave  the  matter  without  express- 
ing my  belief  that  the  term  was  used  by  our  most  expert 
clinicians  to  express  not  blood-pressure,  nor  thickness  of 
vessel  wall,  but  the  relationsliip  between  blood  and  wall 
— the  sustained  fulness  of  the  vessel,  and  so  forth. 

More  recently,  attempts  have  been  made  to  do  away 
with  the  term  "  arterial  tension."  The  present  writer  Was 
amongst  the  first  to  definitely  propose  this,  but  it  is  almost 
impossible  to  get  a  familiar  word  given  up.      Others  have  met 

43 


THE  CLINICAL  ESTIMATION  OF  BLOOD-PRESSURE 

the  difficulty  by  maintaining  that  the  terms  "  tension "  and 
"  pressure,"  are  synonymous.  Personally  I  hold  that  \Yhatever 
conduces  to  clearness  of  thinking  is  desirable,  so  I  am  quite 
ready  to  accept  this  definition  of  the  terms,  but  I  do  not  think 
that  it  is  correct  historically.  It  seems  to  me  that  our  best 
clinicians  meant  more  than  this  indicates,  that  to  them  there 
was  a  living  and  active  relationship  between  the  state  of  the 
vessel  wall  and  the  volume  of  blood  inside  it.  Dr.  Leonard 
Williams,  in  a  lecture  delivered  at  the  Medical  Graduates 
College,  says :  "  High  arterial  tension  is  an  expression  which 
is  used  as  a  synonym  for  '  high  blood-pressure,'  than  which 
it  is  more  euphonious,  but  less  correct."  While  believing,  as 
I  do,  that  our  ablest  clinicians  meant  more  than  is  here 
implied,  the  meaning  of  words  is  frequently  modified,  and 
it  would  greatly  simplify  the  position  were  the  term  "  tension  " 
to  be  given  up,  or  definitely  used  as  synonymous  with  "  blood- 
pressure." 

In  the  examination  of  the  pulse  two  factors  are  com- 
monly considered,  no  matter  what  terms  the  observer  uses  to 
express  his  mental  concept,  namely,  the  condition  of  the 
arterial  wall  and  the  blood-pressure  inside  it.  Putting  aside 
for  the  moment  the  first  of  these,  the  estimation  of  the  pressure 
within  the  artery  is  undoubtedly  taken  as  the  index  of  the 
power  of  the  heart.  The  "  strength "  of  the  pulse  has  no 
meaning  clinically,  save  as  an  index  of  heart  power.  A 
"  feeble "  pulse  means  to  the  chnician  a  feeble  heart ;  a 
"  strong "  pulse  the  reverse.  That  the  pulse  can  reveal 
this  is  the  warrant  for  "  feeling  the  pulse,"  which  is  the 
custom  of  the  clinician. 

The  effect  of  the  blood-pressure  upon  the  arterial  wall 
could,  I  presume,  be  expressed  in  terms  of  "  degrees  of  tension," 
and  it  was  the  cultured  appreciation  of  this  which,  I  believe, 
marked  the  skill  of  our  ablest  physicians  ;  but  it  can  easily  be 
that  the  acquisition  of  this  skill  is  now  regarded  as  too 
difficult,  for  the  internal  pressure,  whatever  it  be,  is  exercised 
upon  tubes  which  vary  in  thickness  of  wall,  in  size  of  lumen, 
and  in  the  relation  of  wall  to  lumen.  The  term  "  tension," 
unless  only  used  as  a  somewhat  rough  indicator,  has  thus  a 
very  subtle  significance. 

Another    aspect    of    this    question    may    l)C    referred    to, 

44 


ARTERIAL  TENSION  AND  BLOOD-PRESSURE 

namely,  the  not  uncommon  use  of  the  term  "  high  tension  " 
to  thickened  radial  arteries.  This  confusion  arose  from  the 
teaching  that  high  blood-pressure  and  thickened  arteries  went 
together ;  so,  when  the  arteries  were  thickened  the  pulse  was 
frequently  spoken  of  as  of  high  tension.  Of  course,  this 
error  was  not  universal,  for  it  was  widely  recognised  that  in 
thick  radials  there  might  l^e  a  feeble  pulse  of  low  blood- 
pressure.  I  refer  to  this  because  it  is  by  recognising  how 
error  originated  that  it  is  most  readily  rectified. 

Senator,  in  a  recent  lecture  on  arterio-sclerosis,  says  that 
in  his  experience  an  increase  in  arterial  tension  is  a  very 
inconstant  factor,  and  depends  greatly  upon  the  condition  of 
the  heart ;  while  the  rigidity  of  the  arteries  places  a  serious 
obstacle  in  the  way  of  determining  the  conditions  of  pressure 
within  them. 

Thickening  of  the  arterial  wall  no  doubt  adds  to  the 
difficulty  of  estimating  the  blood-pressure ;  but  it  is,  I  think, 
not  so  difficult  as  is  the  estimation  of  wall  tension.  As  it  is 
blood-pressure,  in  the  sense  in  which  it  has  just  been  indicated, 
which  is  the  main  object  aimed  at  when  the  pulse  is  examined, 
it  materially  helps  if  this  single  conception  be  kept  before  the 
mind,  and  all  thought  of  "  tension  "  be  abandoned.  That  the 
finger  can  be  educated  to  a  high  degree  of  proficiency  in 
determining  blood-pressure  there  can  be  no  doubt.  What 
has  to  be  acquired  is  the  power  to  estimate  the  pressure 
inside  tubes  of  different  sizes,  and  with  walls  not  only  of 
different  but  of  varying  thickness.  As  we  learn  -  to  dis- 
tinguish between  large  and  small  objects,  as  we  distinguish 
between  a  thick  -  walled  and  a  thin-walled  tube  of  equal 
circumference,  so  we  learn  to  judge  of  the  flow  of  fluid 
through  tubes.  There  is  nothing  more  subtle  or  mysterious 
in  it  than  this,  iDut  it  probably  requires  a  delicate  flnger  and 
much  careful  self-education.  Could  we  introduce  a  cannula 
into  a  patient's  artery,  and  connect  it  with  a  manometer,  a 
record  would  be  obtained  which  would  check  observations 
made  by  the  finger,  and  provide  a  record  the  accuracy  of  which 
would  not  be  questioned.  As  this  cannot  be  done,  methods 
have  been  devised  and  instruments  have  been  constructed 
with  the  object  of  providing  such  records.  In  all  skilled 
work   ingenuity   is   constantly   directed   to   devise   means   of 

45 


THE  CLINICAL  ESTIMATION  OF  BLOOD-PRESSURE 

eliminating  the  individual  equation :  in  the  particular  matter 
with  which  we  are  deahng  it  would  be  of  value  to  be  able 
to  do  this.  It  would  be  of  still  greater  value  could  an 
electrical  balance  be  devised  that  would  correctly  weigh  and 
estimate  the  data  upon  which  a  diagnosis  is  based,  so  that  the 
individual  judgment  and  the  personal  mental  bias  would  be 
eliminated.  We  are,  however,  far  from  this,  and  after  we 
have  counted  blood  corpuscles,  estimated  htemoglobin  richness, 
determined  blood  specific  gravity,  found  the  total  nitrogen 
excretion,  taken  sphygmographic  tracings,  used  the  most  recent 
of  "  blood-pressure  "  instruments,  and  piled  up  a  goodly  array 
of  clinical  data,  the  final  judgment  may  be  no  whit  better. 
The  personal  equation  cannot  be  eliminated  in  diagnosis,  and 
when  it  is  all-important  to  form  a  correct  estimate  of  the 
circulation  as  a  whole,  our  most  recent  methods  still  leave  the 
decision  to  the  individual  acumen  and  experience ;  to  what 
is  nothing  else  than  the  skill  of  the  individual,  determined  by 
inherent  mental  faculty,  developed  by  education  and  en- 
riched by  much  accurate  observation. 

METHODS    OF   ESTIMATING   BLOOD-PEESSURE. 

We  may  now  proceed  to  examine  the  methods  in  use  for 
the  clinical  determination  of  blood-pressure,  to  note  some  of 
the  contentions  based  upon  the  records  so  obtained,  to 
determine  what  data  the  methods  used  really  supply  us  with, 
and  what  practical  use  can  be  made  of  the  data  which  they 
supply.  I  have  no  special  desire  to  pull  down  if  I  cannot 
at  the  same  time  build  afresh,  but  it  is  more  than  time  that 
this  important  subject  were  put  upon  a  sound  foundation,  and 
that  the  errors  with  which  it  threatens  to  be  surrounded,  it 
might  even  be  said  adorned,  should  if  possible  be  checked. 

This  is  not  mere  hyperbole,  for  the  present  position  is 
not  only  curious  but  undesirable.  The  position  is  this  ;  on 
the  one  hand  may  be  placed  the  physiologists  who  have 
accepted  the  instruments  in  use,  and  believe  that  they  give 
an  accurate  --record  of  blood-pressure  ;  along  with  them  there 
are  a  certain  number  of  physicians  who  have  accepted  the 
dictum  of  the  physiologists,  and  have  drawn  important  clinical 
inferences  from  the  risfid  application  of  physiological  methods 

46  "      -.     - 


METHOD^S  OF  ESTIMATING  BLOOD-PRESSURE 

to  pathological  conditions.  On  the  other  hand,  there  ai'e  a 
number  of  physicians  who  have  absolutely  discarded  the 
instruments  in  question,  not  only  as  useless,  but  as  seriously 
misleading.  When  this  is  the  state  of  opinion,  it  is  evident 
that  there  is  something  to  be  found  out,  and  the  matter  is 
so  very  important  from  the  physician's  standpoint  that  I  do 
not  hesitate  to  submit  my  observations  and  conclusions,  in 
the  belief  that  they  can  and  ultimately  will  reconcile  divided 
opinion. 

The  plan  or  principle  on  which  blood-pressure  instru- 
ments are  based  is  simple,  and  may  be  briefly  described.  An 
armlet  made  of  some  strong  material  has  a  rubber  bag 
attached  to  its  internal  surface.  When  this  armlet  is  applied 
and  fastened  by  means  of  straps,  the  rubber  bag  is  blown  up 
by  means  of  a  ball  syringe  attached  to  the  bag  by  rubber 
tubing ;  another  piece  of  rubber  tubing  leads  to  a  manometer 
which  records  the  pressure  of  the  air  inside  the  apparatus  as 
it  is  slowly  pumped  in.  When  the  bag  of  the  armlet  is 
distended  sufficiently  to  grasp  the  arm,  the  index  of  the 
manometer  moves  up  and  down  with  every  arterial  pulse 
wave :  at  a  certain  pressure  the  pulse  wave,  as  seen  on  the 
index  of  the  manometer,  attains  its  maximum  degree  of 
excursion ;  this  point  is  taken  by  some  observers  to  repre- 
sent the  diastolic  loressurc  in  the  arteries.  Other  observers 
use  the  same  kind  of  instrument  in  another  way, — the  bag 
of  the  armlet  is  distended  until  the  arterial  circulation  in 
the  arm  is  stopped  by  the  pressure  of  the  distended  bag,  the 
stoppage  being  judged  of  by  the  finger  on  the  radial  artery,  or 
by  a  second  bag  attached  to  a  wristlet.  The  height  to  which 
the  manometer  index  has  risen  is  taken  as  representing  the 
maximum  or  systolic  pressure.  A  third  method  is  applied  in 
the  construction  of  Gartner's  tonometer  and  corresponding 
instruments.  In  this  method  one  of  the  fingers  is  rendered 
bloodless  by  passing  a  tight  rubber  ring  from  the  tip  of  the 
finger  upwards  along  the  two  terminal  phalanges,  then  a 
rubber  bag  is  passed  round  the  proximal  phalanx  and  distended 
with  air  sufficiently  to  ensure  sufficient  compression  to  pre- 
vent blood  passing  into  the  finger  after  the  rubber  ring  is 
removed ;  the  pressure  in  the  bag  is  recorded  by  a  manometer 
attached    to   it    hj  a   rubber    tube ;    the  pressure   is    slowly 

47 


THE  CLINICAL  ESTIMATION  OF  BLOOD-PRESSLTRE 


lowered,  and  the  point  at  wliich  the  index  stands  when  the 
finger  flushes  is  taken  as  the  systolic  pressure. 

In  the  first  method  the  maximum  pulsation  obtained 
from  the  compressed  vessel  is  taken  as  the  record;  in  the 
second  and  third  methods  the  point  at  which  the  vessel  or 
vessels  are  so  obliterated  as  to  arrest  the  circulation  in  the 
part  is  taken  as  the  record. 

It  is  these  records  which  it  is  maintained  give  the 
"  blood  -  pressure."  After  using  and  comparing  various 
types  of  instrument  in  a  variety  of  cases  it  seems  to  me 
that    those   which   are   used  to    obtain   systolic   pressure   by 


Dr.  Geoi'o-e  Oliver's  hfemomanometer  as  made  by  Mr.  Hawksley,  357  Oxford 
Street,  London,  W.  A  detailed  description  of  the  instrument  and  hov--  to  use 
it  is  supplied  by  the  maker. 

means  of  obliterating  the  brachial  artery,  or  its  branches  in 
the  upper  part  of  the  forearm,  are  the  most  satisfactory. 
They  are  mostly  modifications  of  the  Eiva-Eocci  instrument. 
Personally  I  prefer  Dr.  George  Oliver's  modification  for  two 
reasons :  first,  because  in  the  manometer  a  spirit  index  is 
used  instead  of  mercury,  which  makes  it  more  easily  carried 
about :  and  second,  because  it  has  a  wrist  bag  by  means  of 
which  you  can  see  when  the  pulsation  in  the  radial  artery 
stops,  which  is  less  of  a  strain  upon  the  attention  of  the 
observer  than  using  the  finger,  while  those  around  the  patient 
can  have  the  whole  proceeding  demonstrated  to  them,  which 
is  impossible  when  the  observer  can  only  communicate  what 
his  finger  determines. 

By  the  methods  which  have  Ijeen  described  it  is  apparent 

48 


METHODS  OF  ESTIMATING  BLOOD-PRESSURE 

that  when,  for  example,  the  armlet  is  applied  to  the  upper 
arm,  pressure  is  exerted  by  the  air-pad  upon  all  the  soft 
tissues  of  the  arm,  sufficiently  to  compress  the  brachiar artery, 
so  that  by  obliteration  of  its  lumen  the  pulsatile  movement  is 
arrested  on  the  distal  side  of  the  compression.  It  is  surely 
reasonable  to  claim  that  this  can  Ije  expressed  as  com- 
pressiMlity,  and  that  the  soft  tissues  take  some  share  in  the 
result ;  but  above  all,  it  would  seem  reasonable  to  assume  that 
the  physical  characters  of  the  artery  will  materially  influence 
the  result.  That  it  is  compressibility  which  is  determined 
cannot  really  be  denied ;  and  this  being  so,  it  is  a  matter  of 
common  knowledge  that  the  compressibility  of  a  tube  depends 
upon  the  thickness  of  its  wall,  and  the  relation  l)etween  that 
and  the  size  of  its  lumen.  A  large  tube  with  a  thick  wall 
is  more  easily  compressed  than  a  small  tube  with  the  same 
thickness  of  wall.  And  yet,  plain  as  this  may  appear  to  be,  it 
is  taught  that  the  compressibihty  of  an  artery  is  determined 
wholly  by  the  pressure  of  the  blood  inside  it,  that  the  thick- 
ness or  thinness  of  the  wall  is  a  negligible  factor,  and  that  there- 
fore the  compressibility,  as  measured  by  the  htemomanometer, 
is  literally  "  blood-pressure." 

Janeway,  in  his  well-known  book  on  blood- pressure, 
definitely  states  his  view  as  follows :  "  That  a  sclerotic 
vessel  may  offer  considerable  resistance  to  compression  is  a 
common  beUef  which  I  do  not  think  is  justified." 

It  is  unnecessary  to  single  out  others  by  name,  for  it  will 
be  found  in  most  recent  writings  that  compressibihty  has 
been  assumed  to  be  "  blood-pressure,"^ — no  other  explanation 
or  interpretation  of  records  has  been  given,  so  far  as  my 
reading  has  revealed.  No  doubt,  as  Janeway  says,  there  is  a 
"  common  belief  "  which  is  contrary  to  this,  but  the  object  of 
writers  on  blood-pressure  seems  to  be  either  to  ignore  it  or 
to  assume  that  it  is  one  of  the  common  leliefs  which  possess 
the  minds  of  uninformed  persons. 

Although  the  condition  of  the  arterial  wall  is  so 
definitely  assumed  to  be  a  negligible  factor  in  the  records 
obtained  by  means  of  the  htemomanometer,  it  must  be 
remembered  that,  before  the  instruments  referred  to  came  into 
such  extensive  use,  it  was  fully  recognised  by  the  best 
clinicians  that  the  state  of  the  vessel  wall  was  an  important 
D  49 


THE  CLINICAL  ESTIMATION  OF  BLOOD-PRESSURE 

factor  in  what  was  commonly  known  as  "  compressibility  of 
the  pulse."  It  was,  indeed,  universally  recognised  that  when 
the  wall  was  thickened  the  pulse  was  less  compressible.  If 
the  new  conception  were  correct,  it  would  imply  that  what 
was  formerly  regarded  as  knowledge  was  a  mere  figment 
of  the  imagination,  and  that  all  our  knowledge  about  thin 
and  thick  tubes  appertained  to  the  physical  characters  of 
rubber  tubes,  and  had  no  relationship  to  the  arterial  tube. 
The  revolutionary  nature  of  the  newer  view  seems  to 
have  been  but  partially  realised.  It  seems  to  have  been 
based  upon'  observations  on  normal  walled  vessels,  for  I 
cannot  imagine  anyone  accustomed  to  the  clinical  observa- 
tion of  arteries,  and  equally  familiar  with  the  appearance 
of  the  same  vessels  after  death,  accepting  the  new  view. 
It  is  as  unsound  pathologically  as  it  is  clinically.  If  the 
wall  of  an  artery  can  become  many  times  thicker  than  the 
normal,  the  common  physical  law  must  be  applicable  to  it, — '- 
it  cannot  but  be  more  resistant,  it  cannot  but  require  more 
powder  to  obliterate  its  lumen.  The  normal  radial  artery,  for 
instance,  collapses  by  its  own  weight  when  empty,  while  it  is 
commonplace  knowdedge  in  pathology  that  if  the  wall  of  an 
artery  is  thickened  its  cut  end  gapes.  Certain  physical  pro- 
perties are  as  applicable  to  arteries  as  to  rubber  tubes.  It  is 
indeed  curious  to  note,  on  the  one  hand,  the  application  of  the 
physical  characters  of  rubber  tubing  to  illustrate  and  elucidate 
the  phenomena  of  the  circulation ;  and  on  the  other  hand,  the 
apparent  abandonment  of  all  our  common  knowdedge  of  physics 
when  the  compressibility  of  an  artery  is  imder  consideration. 

As  the  result  of  experience,  I  venture  to  say  that  when  the 
method  of  obtaining  hpemomanometer  readings  is  submitted  to 
the  physicist,  he  will  smile  at  the  suggestion  that  the  readings 
represent  the  pressure  of  the  fluid  inside  the  compressed  vessel. 
This  point  need  not  be  further  elaborated,  and  I  willingly  turn 
from  it  to  the  constructive  side  of  the  subject. 

THE   FACTORS    DETERMINING    H.^:iiIOMANOMETER 
READINGS 

I  submit  that,  by  the  methods  used,  the  light  of  a 
limited  knowledge  of  physics   suggests  that  there  are  three 

50 


HvEMOMANOMETER  READINGS 

factors  to  be  considered — (1)  The  soft  tissues  surrounding 
the  artery ;  (2)  the  arterial  wall :  and  (3)  the  pressure  of 
the  blood  within  it. 

Tissues  surrounding  the  Artery.  —  Taking  up  the 
first  of  these — -the  soft  tissues  surrounding  the  artery — I 
may  at  once  state  that  so  far  as  I  can  see  this  factor  is 
practically  negligible.  I  thought  at  one  time  that  it  might 
prove  to  be  an  important  factor,  but  after  a  careful  comparison 
of  the  girth  of  arms,  whether  due  to  muscularity  or  adiposity 
on  the  one  hand,  or  to  emaciation  on  the  other  hand,  with 
manometer  readings,  I  am  convinced  that  the  factor  is,  as 
I  have  said,  practically  negligible.  Even  the  appUcation 
of  the  pressor  bag  over  the  arm  covered  with  ordinary 
clothing  gives  mucli  the  same  record  as  when  appKed  over 
the  uncovered  arm.  Further,  the  bag  on  the  upper  part  of 
the  forearm  gives  practically  a  like  reading  to  that  obtained 
from  the  upper  arm.  I  therefore  pass  from  this  factor  to  the 
consideration  of  the  other  two. 

Thickness    of   Arterial   Wall. — That  the  thickness   of 
the  wall  of  a  tube,  and  the  proportion  this  bears  to  the  bore, 
affects  its  compressibihty  is    a    fact  of    common  knowledge, 
as  has  been  already  pointed  out.      It  is  one  of  the  beliefs  it 
is    difficult    to    reaUse    should    require    proving.       That    the 
contrary  opinion  exists,  when  the  tubes  are  arteries,  has  been 
already  shown ;    and  it  seems  to  me  that  it  has  arisen  by 
the  rigid  application    to    clinical  and  pathological  problems 
of    the    conclusions    drawn     from     physiological    experiment 
and  observation.      It  has  come  about  in  this  way.      A  normal 
artery  of  such  size  as  the   radial  has   such   a  thin  wall  that, 
when  empty,  it  collapses,  as  a  piece  of  thin  rul^ber  tubing 
collapses ;  if  the  vessel  be  full  of  blood,  or  other  fluid,  its 
walls  are  held  apart,  and  its  lumen  is  maintained.      If  by  any 
device  fluid  pressure  is  exerted  on  the  outside  of  this  full 
vessel  a  very  small  extra  pressure  will  lead  to  its  collapse.     Xo 
matter  what  the  pressiares  be,  the  result  is,  I  believe,  the  same. 
The  wall  is  practically,  if  not  theoretically,  negligible.      That 
similar  results  have  been  obtained  with  arteries  which  have 
undergone  what    I    have    defined    as    arterio-sclerosis    is    to 
be  explained  by  the  entire  loss  of  tone  in  the  dead  vessel, 
so  that  it  is  no  longer  comparable  to  the  living  vessel. 

51 


THE  CLINICAL  ESTIMATION  OF  BLOOD-PRESSURE 

There  is,  of  course,  no  doubt  that  the  arteries  we  examine 
clinically  vary  enormously  in  the  thickness  of  their  wall,  and 
the  relation  of  thickness  of  wall  to  bore.  There  are, 
however,  no  records  of  the  results  of  the  examination  after 
death  of  radial  arteries  known  to  be  thickened  during  life. 
Pathologists  and  clinicians  in  the  post-mortem  room  have 
gone  to  the  aorta  or  the  cerebral  arteries  in  search  of 
atheroma,  and  have  left  the  vessel  felt  during  life  undisturbed 
in  its  resting  place,  and  overlooked  even  amidst  the  yearnings 
of  clinical  curiosity.  This  was  formerly  my  own  position,  but 
in  1 9  0 1  I  drew  attention  to  the  gravity  of  the  omission ;  and 
what  I  wrote  then  and  subsequently  is  the  outcome  of  obser- 
vations which  are  almost  monotonous  in  their  uniformity. 

The  difference  in  the  thickness  of  radial  arteries  and 
in  the  relation  of  thickness  of  wall  to  bore  has  been  shown 
in  Figs.  9  and  11,  and  is  further  represented  in  Figs.  14,  15, 
16,  17,  18,  29,  and  80. 

There  is  no  question  here  of  post-mortem  rigidity,  and 
the  influence  of  fixatives  ;  these  arteries  felt  after  death  as 
they  had  felt  during  life,  save  for  the  absence  of  pulsation 
in  them,  so  that  the  only  question  is  what  changes  led  to 
their  thickening  ?  These  changes  I  have  described  in  an 
earlier  chapter.  No  fixative  treatment  of  normal  arteries 
will  produce  such  pictures  as  I  have  given.  Professor  Mac- 
William  found  that  arteries  taken  from  amputated  limbs  were 
by  stimulation  so  altered  that  their  diameter  could  be 
reduced  to  one-third,  with,  of  course,  a  corresponding  thicken- 
ing of  the  wall.  This  is  a  wide  range  of  contractility  in  a 
normal  vessel,  yet  in  arterio-sclerosis,  where  the  thickening 
encroaches  upon  the  lumen,  and  contractility  is  retained, 
the  diminution  is  still  greater.  Some  of  my  cases  have  shown 
a  thicker  wall  and  a  smaller  bore  than  MacWilliam  records. 
I  cannot  but  think  that  those  who  have  thought  that  the 
vessel  wall  was  negligible  have  not  had  the  data  necessary 
to  a  correct  opinion.  The  following  chapters  will  illustrate 
the  part  taken  by  the  vessel  wall  in  haBmomanometer 
observations.  It  is,  however,  necessary  to  repeat  what 
has  been  said  earlier,  that  thickness  of  the  arterial  wall 
may  be  due  to  two  factors,  separate'  or  combined,  namely, 
permanent  structural  thickening  and  hypertonic   contraction ; 

52 


2   sp 


-5  ^ 


„ 

so 

oT 

<p 

N 

^ 

ai 

o 

"rf 

s 

o 

c3 

CO 

3 

^ 

c5  ;=3   o 


Fig.   17. — Radial  artery,  showing  hypertonic  contraction 
M,  thickened  media;  A,  thickened  adventitia  (xl5). 


Fig.   18. — Radial  artery,  showing  pure  hypermyotro[ihy  and 
hypertonic  contraction. 


HiEMOMANOMETER  READINGS 

and  if  anyone  remains  sceptical  of  the  occurrence  of 
hypertonic  contraction  let  me  again  refer  to  Professor 
Mac  Williams'  observations,  that  in  an  amputated  limb 
the  arteries  could  by  stimulation  be  made  to  contract  so  as  to 
reduce  their  lumen  hj  two-thirds.  I  merely  contend  that 
arteries  do  this  in  the  living  body ;  and  if  clinicians  have  not 
trained  themselves  to  note  its  occurrence  they  will  find  it 
a  most  interesting  study  and  an  invaluable  guide. 

The    Blood-pressure    inside    the    Vessel. — It   is    one 
hundred  and  seventy-five  years  since  Stephen  Hales  introduced 
the  study  of  blood-pressure  iDy  putting  a  tube  into  the  crural 
artery    of    an    animal.      Ninety-five    and    one    hundred    and 
fourteen  years  later,  Poiseuille  and  Ludwig  respectively  con- 
nected a  mercurial  manometer  and  a  writing  style  to  the  tube. 
Others  have  perfected  the  method    thus    begun ;  but    it    is 
unnecessary  to  trace  here  the  stages  of  physiological  evolution 
to  its  present  high  level  of  experimental  exactitude.      It  is 
enough  for  our  present  purpose   to  know  the  conclusions  at 
which  physiology  has  arrived.      Xo  higher  authority  can  be 
found  than  Professor  Leonard  Hill,  and  he  places  the  pressure 
in  the  brachial  artery  of  a  healthy  young  man  at  from  110 
to   130   mm.  of  mercury.      Faivre,  quoted  by  this  authority, 
measured  it  directly  in    man    during    the    amputation  of  a 
limb,  and  his  results  gave  a  pressure  of  from   110   to   120 
mm.   Hg.      This    is    in    close    accordance  with    the  readings 
obtained  by  the  use  of  the  hsemomanometers  already  referred 
to.       My   own    observations   in   persons   with   perfectly   soft 
arteries  place  it  a  little  lower,  namely,  at  from  105  to  115, 
and  not  above   120.      At  this  point,  however,  I  am  in  the 
happy    position     of     being     practically    in     agreement    with 
physiological  teaching.      I  can  draw  further  from  the  same 
source,  but  would  emphasise  the  facts,  namely,  that  during 
sleep  and  when  the  body  is  kept  at  rest,  the  pressure  is  2  0  mm. 
lower ;  and  that  it  rises  2  0  mm.  Hg.  after  violent  exercise. 
It  can  therefore  be  stated  that,  in  the  normal  state  of  living, 
the  pressure  ranges    from    90    to    120;    and    after    violent 
exertion  may  rise  to  140,  this  extra  rise  passing  off  in  about 
fifteen  minutes    after    exertion  stops.      These  figures  closely 
correspond  to  my  own  observations.      I  have,  however,  made 
observations    on    one    active    person  whose    pressure    varied 

53 


THE  CLINICAL  ESTIMATION  OF  BLOOD-PRESSURE 

between  85  and  105,  but  this  is  an  exceptionally  low  record 
for  health. 

On  the  strength  of  the  physiological  statements,  I  submit 
that  the  20  mm.  Hg.  of  rise  after  violent  exercise  marks  the 
limit  of  the  reserve  of  power  of  the  normal  average  heart. 
This  is  the  amount  of  rise  of  pressure  that  the  heart  can  cope 
with  ;  if  raised  somewhat  above  this  the  left  ventricle  would 
give  way,  and  acute  dilatation  would  result,  as  clinically  we 
know  sometimes  occurs.  The  rise  of  pressure  is  not  primarily 
due  to  heart  action,  as  seems  to  be  the  common  conception. 
The  rise  of  pressure  is  due  to  peripheral  constriction  caused 
by  muscular  compression  on  capillaries,  arterioles,  and  even 
arteries  ;  the  inevitable  and  unavoidable  result  being  a  raising 
of  pressure  in  the  larger  arteries  and  the  aorta.  This  raising 
of  pressure  is  purely  mechanical,  and  takes  place  in  a  system 
of  rubber  tubes,  just  as  it  does  in  the  blood  vessels.  The 
living  factor  steps  in  when  the  heart  is  stimulated  to  meet 
this  raised  aortic  and  arterial  pressure  by  increased  work, 
shown  in  more  rapid  and  stronger  ventricular  contractions. 
The  length  of  time  the  left  ventricle  can  maintain  this 
depends  on  the  quality  of  the  individual  heart.  If  the  left 
ventricle  cannot  rise  to  the  aortic  pressure  and  open  the 
aortic  cusps  there  is  a  syncope,  which  may  be  and  often  is 
fatal.  This  may  happen  presumably  with  a  rise  short  of  20 
mm.  Hs.,  and  here  at  the  outset  we  see  that  clinical  medicine 
and  pathology  branch  off  from  the  physiological  standard. 
The  physiological  doctrine  that  a  healthy  young  man  can 
safely  do  what  will  raise  his  aortic  pressure  to  140  mm.  Hg. 
is  accepted,  but  the  two  words  "  healthy  "  and  "  young  "  must 
never  be  omitted  from  the  proposition.  The  observations 
of  clinical  pathology,  however,  are  not  confined  to  the  healthy 
or  the  young,  although  it  seems  as  if  some  people  thought 
that  a  physiological  truth  was  one  of  those  eternal  verities, 
such  as  that  2  +  2  =  4,  applicable  in  all  circumstances  and  at 
all  times.  It  is  not  safe  to  raise  the  blood-pressure  in  all 
aortas  by  this  extra  20  mm.  Hg. ;  and  when  we  get  hfemo- 
manometer  readings  in  man  from  160  to  260,  and  even 
up  to  300,  we  turn  to  physiology  and  ask,  "Is  this  blood- 
pressure  in  the  sense  in  which  you  use  the  term  ?  "  I  know 
that  in   experimental  work  the  aortic  pressure  can  be   some- 

54 


H.EMOMANOMETER  READINGS 

thing  like  doubled  by  constricting  arteries  and  capillaries,  but 
to  prevent  the  heart  coming  to  a  standstill  under  these  con- 
ditions the  vagi  have  to  be  cut. 

In  the  consideration  of  blood-pressure  it  must  be 
remembered  that  the  heart  and  tbe  vascular  system  ha^-e 
a  self-protective  nervous  mechanism.  If  tlie  aortic  pressure 
is  raised  by  systemic  constriction  it  can  be  relieved  by 
splanchnic  dilatation,  and  conversely.  If  the  aortic  pressure 
be  higher  than  the  left  ventricle  can  fully  o\'ercome  the 
residual  blood  in  the  ventricle  is  increased  ;  this  leads  to  over- 
distension ;  over-distension  acts  upon  the  vagal  terminals,  and 
the  heart  is  slowed,  to  give  time  for  the  hypertense  aorta  to 
be  relieved  by  the  passage  onwards  of  more  blood.  The  heart 
is  also  saved  by  blood  accumulating  in  the  veins  when  arteries 
constrict.  In  this  way  it  follows  that  less  blood  reaches  the 
left  ventricle,  and,  as  was  shown  by  Hales  one  hundred  and 
seventy-four  years  ago,  "  the  real  force  of  the  blood  in  the 
arteries  depends  on  the  proportion  which  the  quantity  of  blood 
thrown  out  of  the  left  ventricle  in  a  given  time  bears  to  the 
.  quantity  which  can  pass  through  the  capillary  arteries  into  the 
veins  at  that  time."  The  circulation  has  therefore  very 
efficient  ways  of  preventing  pressure  becoming  too  high,  and 
yet  we  are  told  that  blood-pressure  rises  with  age,  that  in  fact 
high  blood-pressure  is  a  common  sign  of  senility  !  This  is  the 
outcome  of  applying  an  instrument,  evidently  physiologically 
accurate,  all  along  the  line  of  pathological  change,  and  insisting 
that  the  instrumental  readings  continue  to  have  the  same  value. 
I  have  heard  a  physiologist  describe  what  would  happen  if 
blood-pressure  rose  to  300  mm.  Hg.  I  do  not  repeat  his 
words,  but  it  amazed  him  to  be  told  that  such  readings  were 
obtained  from  the  htemomanometer. 

KEFERE^^CES. 

Williams,  Clin.  Journ.,  JSTovember  28  and  December  5,  1906. 
Senator,  i^o?f  a  Therapeutica,  April  1907,  p.  37.  Mac  William,  Phys. 
Proceedings,  June  2,  1906.  Jane  way,  Clin.  Study  of  Blood-Pressiire, 
1904.  Hales,  Staticcd  Essays,  vol.  ii.,  2nd  ed.,  1740,  p.  1  et  seq. 
Poiseuille,  Recli.  sur  la  force  du  cceur  aortique,  Thc'se,  Paris,  1828. 
Ludwig,  Arch,  f  Anaf.  Physiol.,  etc.,  1847. 


55 


CHAPTER   VII 

A  NEW  SCHEMA  OF  THE  CHICULATION 
TO  ILLUSTRATE— 

1.  QUESTIONS    CONCEENING    BLOOD-PEESSUEE. 

2.  THE    INFLUENCE    OF    THE    AETEEIAL    WALL    IN    H^MOMA- 

NOMETEE    EEADINGS. 

Aftee  I  had  arrived  at  what  appeared  to  me  to  be  reasonably 
definite  conclusions  regarding  the  clinical  -phenoioaena,,  Jirst,  of 
hypertonic  contraction  of  arteries  and  its  effect  on  the  blood- 
pressure  in  the  contracted  vessels  ;  and,  second,  of  the  influence 
of  the  arterial  wall  in  hffimomanometer  readings,  it  seemed  to 
me  desirable  to  investigate  these  points  from  the  physicist's 
standpoint. 

I  was  fortunate  enough  to  arouse  the  interest  of  Dr. 
Cargill  Knott,  Lecturer  on  Applied  Mathematics  in  the  Univer- 
sity of  Edinburgh,  in  these  problems,  with  the  result  that  a 
schema  of  the  circulation  was  devised  which  is  represented  in 
the  accompanying  figure.  The  schema  was  the  outcome  of 
much  patience  extended  to  me,  and  of  Dr.  Knott's  technical 
skill  in  his  own  department.  In  its  completed  form  it  seemed 
to  meet  both  his  and  my  requirements. 

The  two  points  to  be  investigated  were — First,  what 
effect  was  produced  by  constriction  of  arteries  upon  the 
pressure  of  fluid  inside  them  ?  Second,  what  part  did  the 
arterial  wall  take  in  determining  arterial  compressibihty,  and 
therefore  in  determining  hasmomanometer  readings.  These 
two  points  seemed  to  me  to  belong  almost  to  pure  physics, 
although  there  were  factors  in  the  living  circulation  which 
they  did  not  embrace. 

The  schema  consists  of  a  glass  reservoir  K^  with  three 
glass  arms  to  which  large  rubber  tubes  are  attached ;  these 

56 


A  NEW  SCHEMA  OF  THE  CIRCULATION 

are  succeeded  by  rubber  tubes  about  the  size  of  the  brachial 
artery :  these  are  again  succeeded  by  larger  tubes  which  are 
attached  to  the  three  g-lass  arms  of  the  second  glass  reservoir 


Fig.  19. — Schema  of  the  circulation  devised  by  Dr.  Cargill  Knott 
and  the  author  ;  description  in  text.  The  thick  tubes  between 
tubes  a,  h,  c  and  R^  and  R-  are  omitted  from  the  figure. 

E-.      On  each  of  the  three  smaller  tubes  two  glass  gauges  M 
are  introduced  to  indicate  the  pressure  inside  the  tubes.      The 


00 


Fig.  20. — Photographs  of  transverse  sections  of  the  three 
tubes  used  in  the  scheme. 

three  tubes  were  made  nominally  of  equal  Ijore,  but  of 
different  thickness  of  wall.  This  ideal  was  not  realised  ;  but, 
as  they  are,  they  suffice  for  our  purpose.  Sections  of  the 
tubes  are  shown  in  Fig.  20, — A  having  the  thinnest  wall,  B 
a  medium  thickness  of  wall,  and  C  the  thickest  wall  with 
the  smallest  bore  or  lumen.  It  will  be  seen,  by  comparing 
these  with  the  sections  of  arteries,  that  there  is  no  greater 
difference  between  the  tubes  than  between  the  arteries. 

Water   is  made  to  flow  through  this  schema  either  by 
means   of   a   syphon  Sy.  connected  with  a  bucket  of   water 

57 


A  NEW  SCHEMA  OF  THE  CIRCULATION 

B.W.,  or  the  thick  rubber  tube  leading  to  reservoir  E^  can  be 
attached  to  a  water  tap.  The  pressure  can  be  regulated  as 
desired,  by  raising  or  lowering  the  bucket,  or  by  means  of  the 
screw  S.  The  pressure  can  be  regulated  by  means  of  the  tap 
when  the  schema  is  attached  to  a  water  pipe.  When  water 
is  flowing  through  this  system  the  two  reservoirs  E^  and  E^ 
ensure  a  uniform  pressure  in  the  three  tubes  a,  h,  c ;  at  all 
events,  the  reservoirs,  in  the  view  of  the  pure  physicist, 
remove  possible  sources  of  fallacy ;  and  this  is  desirable,  as 
the  problems  which  surround  the  flow  of  fluid  through  tubes 
are  very  intricate. 

When  water  is  flowing  through  this  system,  say  from  a 
bucket  of  water,  there  is  a  steady  fall  in  pressure  from  the 
syphon  Sy.  to  the  outlet  D.  This  fall  is  shown  by  the  gauges 
M  on  their  respective  tubes  a,  h,  c.  The  mean  joressure  in 
such  a  system  is  the  average  between  the  highest  and  the 
lowest  pressure,  and  it  is  practically  the  same  in  all  three 
tubes. 

If  now  any  one  of  the  tubes  be  constricted,  no  matter 
how  slightly,  the  pressure  immediately  falls  on  the  distal  side 
of  the  constriction,  and  rises  on  the  proximal  side.  The 
mea7i  pressure  in  the  whole  system  remains  unaltered,  but 
the  distribution  of  the  pressure  is  changed. 

The  scheme  is  so  sensitive  that  touching  any  of  the  tubes 
at  any  point  alters  the  level  of  all  the  six  gauges  ;  the  water 
rising  in  all,  save  the  one  or  two  on  the  distal  side  of  where 
the  finger  is  applied — in  them  the  water  falls. 

It  follotvs  that  in  and  beyond  the  constricted  area  'pressure 
falls ;  above  it,  it  rises.  This  is  a  physical  law,  and  must  be 
as  applicable  to  arteries  as  to  rubber  tubes.  There  appears 
to  be  no  warrant  for  the  view  that  there  is  a  rise  of  blood- 
pressure  inside  constricted  vessels. 

The  second  j^oint  to  investigate  was  the  difference  in  the 
amount  of  pressure  required  to  obliterate  the  lumen  of  the 
tubes  ct,  h,  c,  with  their  different  thickness  of  wall  but  with 
the  same  internal  pressure.  This  was  first  roughly  tested  by 
means  of  weights  applied  over  a  cork  resting  on  the  tubes  in 
succession.  The  cork  was  attached  to  an  upright  rod  kept 
in  position  by  means  of  two  wire  loops  attached  to  a  suitable 
block  of  wood.     Eoughly,  tube  A  required  400  to  500  grains 

58 


A  NEW  SCHEMA  OF  THE  CIRCULATION 

to  obliterate  its  lumen ;  tulDe  B  required  about  1500  grains ; 
and  tube  C  required  about  4000  grains.  The  conditions 
affecting  the  pressure  of  the  fluid  was  uniform  in  all,  and  vet 
there  were  these  enormous  differences  in  the  amount  of  pressure 
required  to  obliterate  the  lumen  of  the  three  tubes.  The 
diameter  of  the  lumen  of  the  tubes  and  the  thickness  of  their 
walls  is  shown  in  Fig.  20. 

It  was,  however,  desirable  to  Ije  somewhat  more  precise 
in  our  observations,  and  I  continued  observations  on  a  new- 
plan.  When  the  pressure  in  the  gauges  was  at  zero,  that  is 
to  say,  when  the  system  was  full,  and  the  water  at  the  foot 
of  the  gauges,  I  attached  a  manometer  to  the  top  of  one  or 
two  of  the  gauges  and  closed  the  tops  of  the  others.  I  then 
turned  on  the  water,  and  found  that  I  could  make  investiga- 
tions with  anv  internal  pressure  I  liked,  so  long  as  it  was  not 
so  high  that  it  burst  the  tubes  or  forcibly  separated  the 
attachments.  I  found  that  I  could  work  conveniently  with 
a  pressure  as  high  as  30  mm.  Hg.  It  then  occurred  to  me 
that  I  had  foimd  a  use  for  the  hsemodynamometer  of  Oliver, 
which,  as  an  instrument  of  clinical  use,  I  had  discarded  for 
his  heemomanometer.  By  means  of  this  instrument  I  could 
with  sufficient  accuracy  determine  in  mm.  Hg.  the  amoimt  of 
pressure  required  to  obhterate  the  respective  tubes. 

Before  giving  the  figures,  I  would  point  out  that  tube  A 
was  so  thin  walled  that  it  collapsed  with  its  own  weight,  as 
a  normal  artery  collapses,  while  the  other  two  tubes  always 
retained  their  round  form. 

The  internal  pressure,  as  shown  by  manometers  attached 
to  the  top  of  some  of  the  gauges  M  while  the  others  were 
closed,  was  30  mm.  Hg.  The  pressure  required  to  obhterate 
the  lumen  of  the  tubes  as  measured  by  the  hsemodynamometer 
was  as  follows  : — 

A  tube  B  tube  C  tube 

10  mm.  Hg.  40  mm.  Hg.  84  mm.  Hg. 

These  numljers  are  at  least  approximately  correct,  and  show 
roughly  the  same  proportion  to  one  another  as  the  rougher 
method  showed. 

It  is  interesting  to  note  that  in  A,  where  the  tulje  was 
only  kept  open  by  the  contained  fluid,  the  lumen  of  the  tube 

59 


A  NEW  SCHEMA  OF  THE  CIRCULATION 

was  obliterated  by  a  directly  applied  pressure  of  10  mm.  Hg., 
while  the  pressure  of  the  flowing  fluid  inside  it  was  30  mm. 
Hg.  It  followed  from  this  that  the  pressure  of  the  flowing 
water  in  the  other  tubes  only  required  to  be  allowed  a  like 
measure;  so  that  in  B  the  tube  wall  equalled  30  mm.  Hg., 
while  in  C  it  equalled  74  mm.  Hg. 

That  this  represented,  at  least  approximately,  the  part 
taken  by  the  wall  of  the  tube,  was  confirmed  by  the  further 
observation  that,  when  the  internal  pressure  was  raised  10 
mm.  Hg.  higher,  the  pressure  required  to  obliterate  the  lumen 
was  also  raised  10  mm.  Hg.  This  observation  was  not 
extended  to  tube  A,  as  a  sustained  internal  pressure  of  40 
mm.  Hg.  found  out  all  the  weak  points  in  that  tube. 

It  appeared  from  these  results  that  the  general  opinion 
was  correct,  that  the  compressibility  of  a  tube  was  determined 
partly  by  the  pressure  of  the  flowing  fluid  inside  it,  partly 
by  the  thickness  of  its  wall,  and  the  relation  between  that 
and  the  lumen  of  the  tube. 

Objection  has  been  taken  to  these  results  on  the  grounds 
that  arteries  are  not  rubber  tubes. 

I  have  made  some  observations  with  vessels  obtained  from 
the  post-mortem  room,  and,  so  far  as  I  have  yet  carried  these, 
they  seem  quite  worthless,  for  the  simple  reason  that  the 
dead  vessel  no  longer  possesses  the  tone  or  the  elasticity  of 
the  living  vessel.  In  fact,  the  rubber  tube  is  a  better 
substitute  for  the  living  artery  than  the  dead  one  is.  It 
may  be  that  when  I  have  the  opportunity  of  testing  some  of 
the  thickened  brachial  arteries  which  I  have  felt  during  life, 
and  which  always  give  a  high  luemomanometer  reading,  I 
may  modify  this  view ;  but  from  what  I  have  seen,  I  am  not 
sanguine  that  the  results  obtained  after  deatli  will  in  this 
particular  lielp  towards  the  elucidation  of  the  clinical 
phenomena. 

A  third  observation  is  worthy  of  being  recorded,  although 
it  had  no  direct  bearing  upon  the  two  points  which  were 
specially  investigated.  The  observation  was  as  follows : — 
Workiag  with  an  internal  pressure  of  30  mm.  Hg.,  when  the 
lumen  of  tube  A  was  obliterated,  the  manometer  on  the 
proximal  side  of  the  point  of  constriction  showed  a  rise  from 
30  to  100  mm.  Hg. ;  the  tube  became  much   distended,  and 

6o 


A  NEW  SCHEMA  OF  THE  CIRCULATION 

gave  way  at  every  weak  poiut.  Tube  B  when  its  lumen  was 
obliterated  showed  a  rise  from  30  to  95  mm.  Hg.  Tube  C 
showed  a  rise  from  30  to  42-2-  i^^i"^-  Hg.  when  similarly 
treated.  These  may  be  tabulated  as  follows,  —  with  an 
internal  pressure  of  30  mm.  Hg.,  when  the  tube  was 
obliterated  there  was  a  rise  of  in 

ABC 

70  mm.  Hg.  65  mm.  Hg.  121  mm.  Hg. 

This  observation  has  considerable  practical  significance. 
In  the  first  place,  it  shows  the  great  rise  in  pressure  that 
would  take  place  in  arteries  the  size  of  the  radial  if  they  did 
not  contract  along  with  the  arterioles  and  capillaries.  The 
relatively  small  rise  that  took  place  in  the  thick- walled  tube 
C  was  very  striking. 

The  phenomena  shown  by  means  of  this  scheme  enable 
us  also  to  understand  very  clearly  the  circulatory  changes 
which  occur  in  the  brain.  The  scheme  can  further  be 
utilised  for  teaching  purposes  to  help  students  to  understand 
and  to  appreciate  the  questions  of  internal  pressure  and  of 
thickness  of  arterial  wall. 


6i 


CHAPTER   VIII 

PRESCLEROSIS  -  HYPERTONUS  VERSUS  BLOOD ^ 
PRESSURE— THE  MODE  OF  PRODUCTION  OF 
ARTERIO-SCLEROSIS 

PRESCLER0SIS-HYPERT0NU8    VERSUS  BLOOD-PRESSURE. 

The  term  Presclerosis  has  been  introduced  by  Huchard  to 
indicate  the  vascular  condition  which  precedes  arterio- 
sclerosis. I  have  already  referred  to  Huchard's  views 
regarding  the  meaning  of  the  term  arterio-sclerosis,  and 
shown  that  he  does  not  separate  the  condition  from 
atheroma,  as  I  contend  must  be  done  if  a  clear  and 
unambiguous  conception  of  the  course  of  arterio-sclerosis  is 
to  be  formed.  It  is  therefore  difficult  to  be  sure  that 
one  is  forming  a  precisely  accurate  estimate  of  his  opinion 
on  certain  points.  He  uses,  for  instance,  the  terms  arterial 
liypertension  and  hlood-overtension  as  synonymous.  I  have  in 
an  earlier  chapter  dealt  with  the  confusion  which  surrounds 
the  use  of  the  former  of  these  terms,  and  it  does  not  seem  to 
me  that  Huchard  has  simplified  tlie  problem.  He  quotes 
with  approval  Mahomed's  study  of  the  pre-albuminuric  stage 
of  Bright's  disease,  in  which  he  recognised  a  functional  period 
characterised  by  blood  hypertension.  Eosenbach  also  is  in 
accord  with  the  view  that  the  thickening  of  the  arterial  wall 
is  the  result  of  the  pressure  of  the  blood.  The  fundamental 
idea  is  increased  blood-pressure,  at  one  time  called  blood- 
hypertension,  at  another  arterial  hypertension ;  while  Dr. 
Leonard  Williams,  who  is  appreciatively  referred  to  by 
Huchard,  and  has  been  referred  to  in  an  earlier  chapter, 
unambiguously  asserts  that  the  terms  are  synonymous.  I 
have  already  expressed  a  doubt  as  to  the  accuracy  of  this,  for 
it    always  appears    to    me    that    the    writings   of    Broadbent, 

62 


PRESCLEROSIS 

Clifford  Allbutt,  and  Huchard  himself  show  that  they  dis- 
tinguished between  the  blood-pressure  and  the  vessel  wall  in 
a  way  that  Leonard  Williams  does  not,  and  that  this  explains 
Broadbent's  belief  in  the  finger  for  the  examination  of  the 
pulse,  while  Williams  regards  it  as  a  most  inept  and  fallacious 
medium  as  compared  with  a  hasmomanometer.  In  fact,  in 
the  writings  on  this  subject  there  is  often  apparent  either  a 
break  in  the  harmony  or  a  false  note,  which  is  unavoidalde 
when  a  factor  is  present  which  is  at  one  point  acknow- 
ledged in  the  abstract  but  ignored  at  a  further  point  in  its 
exposition. 

To  Huchard  the  stage  of  presclerosis  is  the  period  during 
which  there  is  a  continuously  maintained  elevation  of  blood- 
pressure.  So  much  may  be  accepted  as  correctly  interpreting 
his  position,  but  he  follows  others  in  attributing  some- 
what vaguely  the  raised  pressure  to  vessel  constriction.  I 
cannot  better  illustrate  Huchard's  position  than  by  referring 
to  the  discussion  of  a  recent  paper  which  he  submitted  to  the 
Academic  de  Medicine  of  Paris.  In  this  discussion  Lancereaux 
and  Chantemesse  both  denied  that  arterio-sclerosis  was  the 
result  of  hypertension  ;  maintaining,  on  the  other  hand,  that  it 
was  of  the  same  nature  as  the  anatomical  changes  met  with 
in  gout,  rheumatism,  and  lead-poisoning,  that  indeed  "  it  was 
manifestly  of  toxic  origin,"  as  the  latter  of  these  expressed  it. 
No  more  complete  justification  could  be  found  of  my  contention 
that  the  whole  subject  of  arterio-sclerosis,  its  clinical  signific- 
ance, and  the  current  methods  of  estimating  lilood-pressure 
required  clearing  up. 

In  the  discussion  referred  to  it  is  apparent  that 
Lancereaux  and  Chantemesse  confine  their  conception  of 
arterio-sclerosis  to  changes  in  the  tunica  intima ;  while 
Huchard's  conception  of  the  term,  already  dealt  with  in 
Chapter  II.  of  this  book,  is  equally  incomplete.  The  combina- 
tion of  changes  to  which  I  hold  the  term  ought  to  be  confined 
is  nowhere  explicitly  recognised,  and  could  hardly  be,  seeing 
that  the  fundamental  and  primary  phenomenon  of  hypertonic 
contraction  has  been  overshadowed  by  the  idea  of  raised 
blood-pressure. 

Senator  thinks  that  the  early  beginnings  of  arterio-sclerosis 
cannot  be  recognised  clinically  with  certaintv. 

63 


HYPERTONUS   VERSUS  BLOOD-PRESSURE 

THE    MODE    OF    PRODUCTION   OF   ARTERIO-SCLEROSIS. 

The  whole  problem  seems  to  me  to  be  at  once  clarified 
and  simplified  when  we  begin  with  the  first  clinical  step  in 
the  process,  namely,  hypertonic  contraction  of  the  arteries' 
with  which  we  clinically  deal.  It  is  not  that  this  arterial 
contraction  has  been  altogether  ignored,  but  its  pre-eminent 
importance  has  not  been  realised.  Huchard  recognises  that 
toxic  substances  in  the  blood  possess  convulsive  properties 
which  act  on  the  vascular  musculature,  producing  in  the 
arterial  system  a  state  of  spasm  more  or  less  permanent 
which  rapidly  produces  hypertension,  and  consecutively 
arterio-sclerosis ;  but  to  him,  judging  from  his  earlier  writ- 
ings, arterio-sclerosis  is  a  chronic  inflammation  of  the  small 
vessels,  an  endarteriolitis.  He  expressly  states  that  "  arteritis 
of  the  small  vessels  is,  in  short,  the  anatomical  characteristic 
of  arterio-sclerosis."  Broadbent  recognises  peripheral  con- 
traction as  a  cause  of  heightened  blood-pressure.  Allbutt 
fully  recognises  the  correctness  of  the  general  proposition. 

Cotitroversy  has,  curiously  enough,  been  waged  round  the 
question  as  to  whether  or  no  there  is  heightened  arterial 
tension  without  structural  changes  in  the  arteries ;  and  this 
problem  can  be  best  approached  Ijy  indicating  the  order  in 
which  phenomena  appear. 

The  first  step  is  the  presence  in  the  blood  of  toxic 
substances,  or  of  "  muscular  excitants,"  to  borrow  an 
excellent  term  from  Huchard.  These  cause  hypertonic  con- 
traction not  only  of  arterioles  but  of  arteries,  which  have  a 
muscular  coat,  at  least  up  to  the  size  of  the  brachial.  The 
capillaries  often  share  in  the  contraction.  The  presence  of 
this  hypertonic  contraction  is  quite  evident  in  the  radial 
arteries,  the  temporals,  and  other  arteries  within  reach  of  the 
finger.  If  the  muscular  excitants  are  continuously  present  in 
the  blood  the  hypertonus  is  continuous,  and  the  degree  of  the 
latter  must  be  proportionate  to  the  measure  of  the  former. 
The  effect  of  this  tightening  up  of  the  arterial  wall  on  blood- 
pressure  has  been  already  discussed ;  it  leads  to  an  increase 
of  pressure  in  the  aorta,  and  it  does  this  without  any  increase 
in  heart  action ;  although  an  increase  is  called  out,  if  there 
be  any  reserve,  to  overcome  the  greater  difficulty  of  opening 

64 


PRODUCTION  OF  SCLEROSIS 

the  aortic  cusps.  That  there  is  an  equal  raising  of  pressure  in 
the  constricted  vessels  themselves  is  an  altogether  different 
question.  The  constricted  vessels  offer  greater  resistance,  so 
that  less  blood  flows  through  them  and  less  reaches  the 
capillaries.  The  conception  has  been  that  the  increase  in 
pressure  compensated  for  the  constriction,  and  kept  up  the 
blood  supply  in  the  constricted  area,  whereas  what  really 
occurs  is  that  the  constriction  throws  the  increase  of  pressure 
back  on  the  non-constricted  vessels  and  on  the  aorta.  The 
arterial  system  being  made  up  of  sections,  and  the  heart  having 
a  self-regulating  mechanism,  the  increase  of  aortic  pressure  is 
determined  by  the  extent  to  which  constriction  is  general,  and 
by  the  reserve  of  powder  in  the  heart.  That  arterial  contraction 
raises  blood-pressure  by  from  100  to  200  per  cent,  in  the  con- 
stricted vessels  is  the  outcome  of  the  belief  that  the  haemo- 
manometer  under  all  conditions  only  registers  blood-pressure. 
The  recurrence  or  continuance  of  the  hypertonic  con- 
traction leads  to  hypertrophy  of  the  muscular  coat  of  the 
arteries.  That  hypertrophy  occurs  has  been  shown  by 
George  Johnstone,  Savill,  and  myself.  That  the  degree  of 
it  is  influenced  by  the  measure  of  the  blood-pressure  is  more 
than  probable.  Mere  contraction  of  vessels  does  not  lead 
to  hypertrophy,  but  does  so  if  long  continued  and  if  the  blood- 
pressure  be  fairly  maintained.  But  let  me  repeat  that  the 
maintenance  of  blood-pressure  depends  upon  the  power  of 
the  left  ventricle.  This  explains  the  production  of  thickened 
vessels  in  vigorous  people,  and  comparatively  early  in  life. 
These  are  the  people  who,  when  they  are  seen  early  enough, 
have  thickened  and  well-filled  arteries,  but  in  whom  under 
appropriate  treatment  the  thickening  may  disappear.  If  it 
does  not  disappear  it  is  structural.  When  hypertonus 
persists  it  must  lead  to  hypertrophy,  hypertrophy  being 
the  normal  result  of  such  a  condition.  In  my  own  observa- 
tions, when  the  condition  was  permanently  established,  I 
found  that  not  only  was  there  this  thickening  of  the  media, 
but  a  thickening  of  the  intima  also,  and  sometimes  of  the 
adventitia  in  addition.  The  thickening  of  the  intima  is  the 
result  of  a  long-continued  irritation  of  its  tissue  by  substances 
present  in  the  blood.  Savill  does  not  seem  to  have  noted 
this  intimal  thickening  in  his  cases  ;  while  the  French 
E  65 


HYPERTONUS  AND  SCLEROSIS 

school  is  strong  on  intimal  thickening,  and  says  nothing  about 
the  media.  Senator  thinks  that  when  arterio-sclerosis  can  be 
recognised  clinically,  it  is  extremely  probable  that  all  three 
coats  are  affected  ;  but  then  he  does  not  separate  atheroma 
from  his  conception  of  arterio-sclerosis ;  and  in  atheroma  all 
three  coats  are  affected,  but  very  differently  to  arterio- 
sclerosis. It  seems  to  me  that  this  failure  to  separate  the 
two  pathological  conditions  of  atheroma  and  arterio-sclerosis  has 
prevented  clinicians  realising  the  significance  of  processes 
constantly  going  on  under  their  fingers  and  eyes. 

The  physiological  corner-stone  of  my  contention  is  that 
the  vessels  contract  under  the  direct  influence  of  irritating 
substances  present  in  their  contained  blood.  The  same  sub- 
stances act  upon  the  intima.  The  development  of  hyper- 
trophic and  of  hyperplastic  thickening  is  the  result,  and 
has  its  analogue  in  other  situations. 

The  controversy  as  to  whether  a  rise  of  blood-pressure 
precedes  or  follows  vascular  change  becomes  thus  one  of  those 
circular  arguments  to  which  there  is  no  end  until  the  true  steps 
of  the  process  are  determined.  As  in  many  morbid  processes, 
the  first  step  is  an  exaggeration  of  a  normal  process,  and  in  the 
matter  at  present  under  consideration  it  is  seen  in  tonus  becom- 
ing hypertonus ;  the  blood-pressure  in  the  hypertonic  arteries 
not  being  determined  by  the  constriction,  but  by  the  state  of 
tonus  of  other  vessels,  and  by  the  power  of  the  heart.  There 
is  no  absolute  sequence ;  for  although  hypertonus  is  the  fore- 
runner of  sclerosis,  sclerosis  need  not  follow  hypertonus.  But  I 
cannot  imagine  substances  in  the  blood  producing  wide  hyper- 
plasia of  the  tunica  intima  and  not  causing  prolonged  hypertonic 
contraction  of  the  media,  and  its  consequential  hypertrophy. 

The  term  presclerosis  is  as  undesirable  when  applied  to 
the  arteries  as  preliypertrophy  would  be  applied  to  the  heart. 
It  belongs  to  the  pseudo  and  para  type  of  term,  which  is  not 
regarded  with  scientific  favour.  The  adoption  of  such  terms 
tends  to  obscure  truth,  and  even  for  the  time  to  lull  inquiry. 

References.  , 

Mahomed,  Med.-Chir.  Trans.,  London,  1874.  Rosenbacli, 
Breslauer  Artzl.  Zeitsch.,  1886.  Huchard,  "Maladies  du  Coeur  et 
des  Vaisseaux,"  1893,  p.  96  ;  loc.  cit.,  p.  151.  Huchard,  Presderose, 
Bui.  de  I'Academie  de  Med,  Tome  Ivii.,  No.  3,  Seance  du  15  Jan.  1907. 

66 


CHAPTEK   IX 

THE  PRACTICAL  APPLICATION  OF  THE 
PRECEDING  CONCLUSIONS 

VESSEL    SENSITIVENESS    AND    THE    CLINICAL    SIGNIFICANCE    OF 

HYPERTONUS. 

THE    INTEKPRETATION    OF    H^MOMANOMETER    READINGS. 

In  the  preceding  chapters  conckisions  have  been  arrived  at, 
the  practical  significance  of  which  it  is  desirable  to  formulate 
at  this  stage,  as  it  will  make  the  teaching  of  the  later 
chapters  easier  to  follow. 

First — I  have  defined  my  use  of  the  term  Hypertonus  ; 
and  indicated  the  change  in  the  arterial  wall,  and  the  diminu- 
tion in  the  vessel  lumen  which  characterise  it. 

Second — It  has  been  shown  that  hypertonic  contraction 
is  caused  by  the  presence  of  substances  of  various  kinds  in 
the  blood. 

Third — It  has  been  argued  that  continued  hypertonus 
leads  to  hypertrophy  of  the  tunica  media ;  that  this  is 
commonly  associated  with  thickening  of  the  other  two  coats ; 
and  that  the  term  arterio-sclerosis  ought  to  be  confined  to 
these  changes. 

Fourth — The  relationship  between  vessel  contraction  and 
l^lood-pressure  has  been  considered,  and  various  errors  have 
been  dealt  with. 

Fifth — It  has  been  indicated  that  sclerosed  vessels 
retain  their  contractility,  and  are  not  the  rigid  tubes  they 
are  commonly  described  as  being. 

Sixth — The  instruments  used  to  measure  blood-pressure 
only  do  so  in  normal  vessels ;  in  thickened  vessels  the 
readings  are  largely  influenced  by  the  arterial  wall. 

Seventh — As  will    be    shown    subsequentlv,    in    arterio- 

67 


APPLICATION  OF  PRECEDING  CONCLUSIONS 

sclerosis  hsemomanometer  readings  rise  with  hypertonus  of 
the  sclerosed  vessels,  and  fall  with  its  reduction,  but  thick- 
walled  arteries  never  give  normal  readings. 

Eighth — The  ha^monianometer  can  supply  a  record 
which,  as  will  be  apparent  later,  is  not  only  of  interest,  but 
of  clinical  value,  when  properly  interpreted. 

The  following  chapters  taken  from  my  clinical  observa- 
tions are  used  to  illustrate  my  various  contentions ;  but 
before  passing  to  them  I  desire  to  direct  attention  to  what 
may  be  regarded  as  vessel  sensitiveness  under  the  following 
head : 

VESSEL   SENSITIVENESS   AND    THE    CLINICAL 
SIGNIFICANCE    OF   HYPERTONUS. 

It  is  probable  that  vessel  sensitiveness  varies  greatly 
in  individuals ;  judging,  indeed,  by  the  recognised  differences 
in  the  tissues  and  organs  generally  of  different  persons,  we 
are  entitled  to  hold  that  like  differences  exist  in  the  vascular 
walls.  The  recognition  of  this  is  of  practical  importance,  for 
it  leads  us  not  to  look  at  the  vessels  as  a  mere  mechanical 
system  of  tubes,  the  pulse  in  which  indicates  the  degree  of 
heart  power,  but  to  form  our  estimate  of  the  individual  by 
recognising  the  state  of  his  vessels.  Looking  at  the  patient 
with  a  true  picture  of  his  vascular  system  before  our  minds, 
our  estimate  will  assuredly  be  more  correct.  In  fact,  no 
reliable  estimate  is  possible  without  such  a  mental  picture. 
A  persistent  hypertonus,  for  example,  is  abnormal,  and  if  its 
presence  is  recognised  it  will  lead  us  to  appreciate  symptoms 
which  might  otherwise  be  regarded  as  wholly  fanciful. 
Such  symptoms  associated  with  vascular  manifestation  are 
often  the  first  steps  and  the  beginnings  of  processes  which 
become  permanent  anatomical  changes.  Eegrets  are  from 
time  to  time  expressed  that  we  do  not  know,  do  not  see,  the 
beginnings  of  morbid  processes ;  that  we  only  know  them 
when  fully  established.  Here,  as  in  all  other  departments 
of  life,  we  only  see  what  w^e  have  eyes  to  see.  The  coarse, 
the  sudden  accidents  which  befall  man  necessarily  first 
attract  attention ;  the  coarse  results  of  disease  long 
occupied  men's   minds :    it   is    only  now   that   we  are   in   a 

68 


VESSEL  SENSITIVENESS 

position  to  appiehend  the  subtle  modifications  which  lead  to 
manifestations  which  were  deemed  unimportant,  if  recognised 
at  all,  a  relationship  which  it  is  now  our  privilege  to  recognise, 
at  least  in  some  degree,  and  to  make  some  useful  application 
of  our  knowledge. 

The  position  in  outline  is  this :  the  individual,  with  his 
physical  and  mental  endow^ments,  the  expression  of  his 
heredity  and  environment,  feeds  himself.  His  tissues  and 
organs  are  nourished  by  a  nutrient  fluid  whose  intimate 
and  subtle  composition  is  determined  by  heredity,  by  what 
he  eats,  and  by  the  activity  or  efficiency  of  his  excretory 
functions.  Even  these  last  may  be  largely  hereditary,  or, 
what  is  equivalent  to  it,  congenital.  The  hereditary  factor 
is  the  characteristic  of  the  individual,  his  "  constitution,"  his 
special  and  peculiar  chemico-vital  composition :  to  what 
extent  it  can  be  altered  is  still  a  much  debated  question. 
This  factor,  it  may,  however,  be  safely  said,  is  more  or  less 
permanent ;  but  its  manifestations  depend  upon  the  pabulum 
supplied  to  it.  The  man  who  is  congenitally  what  we  call 
gouty  will  assuredly  manifest  his  heredity  under  certain 
feeding  conditions,  and  will  not  do  so  under  other  conditions. 
His  heredity  may  remain  in  abeyance ;  whether  it  can  be 
eliminated  by  prolonged  abeyance,  whether  it  might,  so  to  say, 
disappear  from  never  being  called  out,  is  a  problem  difficult 
to  determine  with  rigid  accuracy.  In  this  connection  it  may, 
however,  be  remarked  that  people  who  once  show  idiosyncrasy 
do  not,  in  my  experience,  lose  it.  Persons  who  get  urticaria 
from  eating  shell  -  fish  manifest  their  idiosyncracy  right 
through  life.  An  old  friend  of  mine  continued  to  Ije  poisoned 
by  egg  in  the  smallest  quantity  up  to  the  time  of  his  death 
at  four-score  years ;  a  lady,  well  on  in  middle  life,  lost  in  no 
degree  the  severity  of  the  symptoms  of  spinal  cord  poisoning 
which  infusion  of  ordinary  tea  induced  in  her.  So  through- 
out the  whole  mass  of  individuals  there  is  this  personal 
factor ;  and  equally  in  the  individuals  with  whom  we  have 
to  deal  this  hereditary  factor  can  be  modified,  can  be  helped, 
strengthened  or  restrained  by  the  composition  of  the  blood. 
Not  that  the  blood-forming  organs  are  altered,  l)ut  their 
working  is  and  must  be  modified  by  the  blood  supplied  to 
them ;  while   outside   the  indirect   contributions   from    those 

69 


SIGNIFICANCE  OF  HYPERTONUS 

organs  the  blood  depends  directly  upon  the  feeding.  But 
the  blood  channels  are  not  only  the  conduits  for  carrying 
nourishment,  for  supplying  the  raw  material  from  which 
various  elements  and  ingredients  of  the  blood  itself  are 
manufactured ;  they  are  also  the  sewers  of  the  body,  taking 
away  the  waste  from  every  cell  and  organ.  The  efficiency 
even  of  this  function  may  be  determined  by  heredity,  for  it 
depends  upon  the  thoroughness  of  the  metabolic  and  katabolic 
processes  in  the  individual  cell, — that  is,  upon  its  inherent 
vigour.  We  may  not  be  able  to  greatly  increase  that  vigour, 
but  we  can  do  much  to  prevent  its  being  paralysed  by  an 
excessive  call  for  work.  If  we  understand  the  scheme  right 
we  can  prevent  the  low-vigour  cells  being  deluged  with 
pabulum,  which  not  only  they  cannot  utilise,  but  whicli 
smothers  the  power  they  do  possess.  The  medical  problem 
circles  round  the  three  factors  of  hereditary  character, 
pabulum,  and  excretion.  Fortunately,  the  pabulum  conduits, 
which  it  must  be  realised  are  also  the  sewage  conduits,  are 
not  mere  elastic  tubes,  but  living  tubes,  responding  to  the 
composition  of  the  contained  blood,  narrowing  their  calibre 
when  the  blood  contains  some  hurtful  substances,  dilating 
when  paralysed  by  other  substances.  That  this  property 
of  direct  response  on  the  part  of  the  vessel  wall  .to  the 
composition  of  the  blood  has  for  its  object  the  protection  of 
the  tissues  seems  to  me  to  be  its  true  explanation ;  it  takes 
away  the  purely  physical  conception  of  the  circulation,  and 
raises  our  conception  of  it  to  a  level  with  our  conception  of 
other  systems. 

We  thus  come  to  the  conclusion  that  sustained  hyper- 
tonus  indicates  the  continued  presence  of  substances  in  the 
blood  which  act  by  irritating  the  vessel  walls,  leading  to 
their  hypertonic  contraction.  These  substances  betray  their 
hurtfulness  by  their  action,  for  sustained  hypertonus  is  hurt- 
ful :  it  raises  peripheral  resistance  and  keeps  it  unduly  high  ; 
it  prevents  the  peripheral  flushing  with  blood  which  is 
required  for  full  cell  vigour,  and  for  the  complete  removal 
of  refuse  and  waste. 

This  is  a  large  generalisation,  and  yet  it  is  no  sooner 
put  into  words  than  its  truth  is  apparent.  The  knowledge 
we  already  possess  warrants  us  in  regarding  this  as  a  fact — 

70 


HYPERTONUS  IN  OLD  PEOPLE 

as  a  law— as  the  fundamental  fact  on  which  a  correct  con- 
ception of  the  relationship  between  metabolism  and  the 
circulation  is  to  be  based.  It  becomes  a  new  guide  to  us, 
an  indicator  of  the  more  subtle  changes  taking  place  in  the 
fluid  upon  which  health  and  vigour  depend. 

This  is  not  only  true  of  normal  vessels,  it  is  true  of 
sclerosed  vessels ;  their  tightening  up  inclieates  the  presence  of 
deleterious  substances  in  the  hlood,  they  relax  as  these  are 
removed.  The  proposition  that  sclerosed  vessels  can  be 
more  sensitive  than  normal  vessels  to  such  influences  has 
been  a  difficulty  with  some  of  my  friends,  yet  it  has  been 
shown  by  the  physiologists  that  vessels  become  more 
sensitive,  acquire  an  "  exaggerated  irritability,"  to  some  of 
the  constrictor  substances,  referred  to  in  previous  chapters, 
after  degenerative  section  of  the  vasomotor  nerves.  It 
seems  to  me  that  in  the  sclerosed  vessels  of  old  people  this 
extreme  sensitiveness  is  sometimes  very  marked,  and 
although,  as  I  have  stated  in  Chapter  IV.  page  29,  there  are 
certain  possible  fallacies,  there  is  no  doubt  as  to  the 
existence  of  this  extreme  sensitiveness,  and  that  it  persists 
after  nerve  impulses  have  clearly  become  dulled.  The 
recognition  of  this  is  of  immense  importance,  for  arterio- 
sclerosis may  be  unaccompanied  by  symptoms  requiring 
medical  skill,  whereas  the  advent  of  hypertonus  always 
heralds  symptoms  referable  to  one  or  other  organ.  The 
hypertonus  becomes  thus  an  indicator  of  blood  condition,  not 
of  nerve-centre  perturbation.  The  brain  perturbation,  when 
present,  is  of  vascular  origin. 

THE  INTERPRETATION  OF  H^MOMANOMETER  READINGS: 
ANGIOHiEMOMANOMETER  OR  ANGIOMANOMETER. 

From  what  has  been  said  in  previous  pages  it  will  have 
become  apparent  that  my  contentions  lead  to  the  conclusion 
that  the  two  factors  in  the  determination  of  arterial  pressure 
or  compressibility,  as  measured  by  the  instruments  in  use,  are 
(1)  hloocl-pressure,  and  (2)  the  thickness  of  the  vxdl  and  the 
IJTOiJortion  it  bears  to  the  lumen. 

When  observations  are  made  on  persons  with  soft  and 
absolutely    unthickened     vessels    the    arterial    pressure    ap- 


INTERPRETATION  OF 

parently  corresponds  with  the  pressure  that  would  be 
obtained  were  a  cannula  introduced  into  the  artery.  In 
such  persons  there  is  a  rise  and  fall  of  pressure  equal  to 
about  20  mm.  Hg.  in  the  24  hours.  I  do  not  doubt  that 
there  is  this  measure  of  variation  in  true  blood-pressure.  I 
do  not  question  the  proposition  that  the  instrumental 
readings  record  this,  and  that  in  the  normal  daily  variations 
the  state  of  the  vessel  wall  may  be  negligible ;  and  yet  it 
will  commonly  be  found  that  the  higher  readings  coincide 
and  correspond  with  some  hypertonic  contraction  of  the 
vessel  wall.  As  soon,  indeed,  as  readings  go  above  normal, 
it  will,  in  the  vast  majority  of  instances,  be  found  that  they 
are  accompanied  by  a  definite  thickening  of  the  radial 
wall,  and  that  the  fall  in  pressure  coincides  with  the  soften- 
ing and  relaxation  of  the  artery,  and  corresponds  with  it. 

The  artery  we  depend  upon  for  our  finger  observations 
is  the  radial,  while  the  vessel  compressed  is  the  brachial ; 
and  it  is  well  to  bear  in  mind  that  the  condition  of  the  wall 
of  the  brachial  is  not  always  duplicated  in  the  radial,  or 
vice  versa ;  in  the  great  majority  of  instances  it  is  so,  but  one 
meets  with  exceptions  on  both  sides,  sufficiently  few,  however, 
to  prove  that  correspondence  is  the  rule. 

When  the  radial  is  thickened  from  structural  changes 
the  pressure  remains  constantly  above  normal ;  the  degree 
of  thickening  and  its  proportion  to  the  size  of  the  lumen 
determining  the  height  of  the  instrumental  reading.  When 
a  thick  vessel  tightens  up  in  hypertonus  the  reading  increases 
by  from  20  to  40  mm.  Hg.  or  more,  and  falls  as  it  is  relaxed. 

The  fact  that,  with  a  thick  vessel  wall,  the  reading 
often  never  falls  below  say  200  mm.  Hg.,  no  matter  how 
poor  the  power  of  the  wave  inside  the  vessel  may  be,  and 
no  matter  what  means  be  taken  for  the  reduction  of  the 
reading,  is  really  an  absolute  proof  that  the  vessel  wall 
takes  a  large  share  in  the  resistance  to  the  compressing  bag. 
That  being  so,  it  necessarily  follows  that  the  vessel  wall, 
save  in  the  perfectly  normal  vessel  which  is  only  open  when 
it  is  full  of  blood,  has  to  be  reckoned  with.  The  contrary 
contention  has  entirely  discredited  the  use  of  the  hsemomano- 
meter  with  many  accomplished  clinical  pathologists,  and  the 
result  is  not  to  be  wondered  at. 

72 


H.EMOMANOMETER  READINGS 

When  it  is  recognised  that  the  arterial  wall  is  such  an 
important  factor  it  will  be  found  that  some  moderately  high 
pressures,  say  140   to   150   mm.  Hg.,  are  due  to  hypertonic 
thickening,  and  that  both  pressure  reading  and  thickness  of 
wall  can  be  easily  reduced  to  normal ;  that  in  other  instances 
still  higher  pressures,  say  220   to   240   mm.  Hg.,  can  never 
be  reduced  to  normal,  but  that  a  lowering  of  20  to  40  mm. 
Hg.,  or  rather  more,  may  be  induced,  and  that  it  corresponds 
with  a  measure  of  wall  relaxation  which  is  readily  appreci- 
able to  the  finger.     The  fall  is  the  result  of  the  relief  of  the 
hypertonus.      I  have  already  said  it  is  the  hypertonus  which 
is  the  essential  phenomenon ;  and  as  hypertonic  contraction 
still  further  thickens  the  wall  and  reduces  the  lumen  of  a 
sclerosed  vessel,  the  reading  must  be  raised  under  the  circum- 
stances, and  will  fall  with  the  disappearance  of  the  hyper- 
tonus.     I  do  not  believe  that  any  who  have  the  abundant 
opportunities  of  carefully  watching  thick  vessels  that  I  have, 
will  have  any  serious  difficulty  in  satisfying  themselves  as 
to    the   correctness   of   these  statements.      I  must,   however, 
again   add   a  warning   note  to    the    effect   that   feeling   the 
radial  is  not  always  a  reliable  guide  as  to  what  the  brachial 
pressure  is  to  read.      I  have  already  referred  to  this,  and  I 
shall  only  add  that  in  some  cases  the  radial  artery  and  its 
■pulse    would    not    lead    one    to    suppose    that    the    brachial 
pressure    would    be    high.     I    have    two   such    cases    under 
observation  as  I  write  this,  the  radial  artery  being  neither 
hard     nor     incompressible,    and    yet    in     both    there     is    a 
steady  reading  from  the  brachial  of  over  200  mm.  Hg.     In 
another     case,    also    under    present     observation,    in    whom 
frequently  repeated  doses  of  erythrol  dilated  the  capillaries 
so  that  the  patient  became  ruddy  in  appearance  instead  of 
pale    and    haggard   looking,   and   yet   his   brachial   pressure, 
which  was  over  200.  was  not  reduced.      On  the  other  hand, 
the  brachial  pressure  may  be  lower  than   the   state   of  the 
radial  suggests.      I  have  seen  calcareous  radials  the  pulse  in 
which  was  stopped  by  a  brachial  pressure  of  200,  while  had 
the  brachial  been  like  the  radial  its  wall  could    only  have 
been  compressed   by  splintering   it.      One   other   reservation 
has  to  be  made,  namely  this,  that  occasionally  a  pressure  of 
110   mm.  Hg.  will  become   120   by  relaxing  the   vessels — 

73 


H.^MOMANOMETER  READINGS 

the  wave  in  the  radial  becoming  larger  and  more  vigorous. 
I  have  not  seen  many  instances  of  this,  and  at  first  they 
were  perplexing,  but  the  explanation  seemed  to  me  to  be 
clear,  namely,  that  the  relief  of  hypertonus  freed  the  heart 
and  allowed  it  to  act  with  so  much  greater  vigour  that  the 
loss  from  the  change  in  the  vessel  wall  was  more  than 
balanced  by  a  true  rise  in  blood-pressure. 

I  mention  these  apparent  exceptions  to  the  propositions 
I  have  submitted,  for  I  believe  that  their  occurrence  has  mis- 
led observers.  I  acknowledge  the  difficulty  they  presented 
to  myself,  but  steady  and  close  observation  in  due  time  solved 
the  riddle,  so  far  as  I  was  concerned. 

Were  I  ambitious  to  add  another  word  to  the  rich  new 
vocabulary  in  medicine,  I  would  suggest  angioJue  mo  memo  meter 
as  a  further  development  of  the  word  haemomanometer,  or 
angiomanomcUr  as  a  satisfactory  substitute  for  hsemomanometer. 

EEFERENCE. 

Elliott,  loc.  cit. 


7A 


CHAPTER   X 

HYPERTONUS  AS  SHOWN  BY  THE 
SPHY^GMOGRAPH 

The  followiug  four  cases  are  representative  of  classes  of  cases. 
They  all  showed  hypertonic  thickening  of  the  radial  arteries 
when  they  came  under  observation,  and  they  were  all  treated 
by  anti-spasmodics  with  a  view  to  the  relief  of  arterial 
hypertonus.  The  results  of  the  treatment  on  the  arteries  are 
shown  in  the  sphygmographic  tracings. 

Case  2.^ — A  man,  aged  35  years,  came  to  me  at  the 
Edinburgh  Royal  Infirmary  complaining  of  headache  and 
general  weakness  and  insomnia.  He  was  a  strongly-built, 
well-nourished  man,  but  was  somewhat  pale.  He  had  been 
working  at  his  present  occupation  for  three  months,  and 
before  that  time  had  been  well.  The  radial  artery  was 
markedly  thick,  the  thickening  being  uniform  and  extending 
right  up  the  arm.  In  fact,  it  presented  the  characters  which 
would  commonly  be  described  as  "  arterio-sclerotic."  The 
man  was  young,  and  this,  combined  with  his  symptoms  and 
the  absence  of  any  evidence  in  the  urine  of  renal  disease,  led 
me  to  surmise  that  this  vessel  condition  was  largely  one  of 
hypertonus  and  that,  even  assuming  that  there  might  be 
some  degree  of  thickening,  his  complaints  were  due  to  the 
hypertonus  and  to  the  cause,  whatever  it  might  be,  producing 
it.  A  sphygmographic  tracing  was  taken,  and  he  was 
admitted  into  Ward  23.  Some  doses  of  erythro-tetranitrate 
demonstrated  that  hypertonus  was  accountable  for  most,  but 
not  all,  of  the  radial  thickening ;  this  druo',  while  relaxino- 
arterial  spasm,  does  not,  of  course,  remove  an  organised 
thickening.      In  this  case  the  thickening  was  greatly  reduced 

75 


HYPERTONUS  AS  SHOWN  BY  SPHYGMOGRAPH 

by  relaxing  the  spasm.      The  sphygmographic  tracing  may  be 
compared  with  the  former  one.      The  existence  of  hypertonus 


Fig.  21. — Before  erythrol. 


Fig.  22.— After  erythrol. 


in  this  case  was  of  special  interest,  as  we  found  afterwards 
that  the  man  had  had  syphilis. 

Case  3. — The  following  tracings  were  also  from  a  patient 
in  Ward  23  suffering  from  spasmodic  asthma.  He  was  a 
man,  aged   53   years,  and  it  was  quite  clear  that  when  the 


Fig.  23. — Before  liquor  trinitriiii. 


Fig.  24. — After  liquor  trinitriui. 

asthmatic  spasm  supervened  Jiis  radial  arteries  became 
markedly  tightened  up.  The  following  are  tlie  pulse 
tracings  during  the  asthmatic  spasm,  and  after  its  relief  by 
means  of  liquor  trinitrini. 

76 


HYPERTONUS  AS  SHOWN  BY  SFHYGMOGRAPH 

Q^SE  4. — These  tracings  were  from  a  man,  aged  about 
60  years,  also  in  Ward  23,  suffering  from  extreme  orthopnoea, 
due  to  myocardial  degeneration.     The  vessels  were  thickened, 


Fig.  26. — After  relaxation  of  radial  artery. 


but  they  also  seemed  to  me  to  be  in  a  condition  of  hypertonus. 
He  got  great  relief  from  the  administration  of  anti-spasmodics 
which  relaxed  his  vessels. 

Case  5. — The  next  tracings  were  from  an  old  man,  aged 
70  years,  who  was  under  my  observation  for  years  in  Queens- 


FiG.  27. — Duriiie'attack  of  "renal  asthma." 


Fig.  28. — In  intervals  of  attacks. 

berry  House.  He  was  subject  in  his  later  years  to  recurring 
attacks  of  "  renal  asthma,"  during  which  his  permanently 
thickened  vessels  quite  appreciably  tightened  up  andj^became 

n 


HYPERTONUS  AS  SHOWN  BY  SPHYGMOGRAPH 

thicker.  The  sphygmograph  gave  the  following  tracings 
during  the  attacks  and  in  the  intervals. 

In  these  four  cases  the  difference  in  the  pulse  when 
tightened  and  not  tightened  was  quite  appreciable  to  the 
finger.  The  sphygmograms  entirely  bear  this  out.  Under 
hypertonus,  with  the  well-filled  thick-walled  artery,  the  swing 
of  the  lever  is  less,  the  percussion  stroke  is  shorter  and  Ibss 
abrupt,  the  summit  tends  to  be  more  rounded,  and  the  pre'di- 
crotic  notch  less  evident.  When  the  hypertonus  passes  off  all 
this  is  altered. 

In  the  chapters  which  follow  I  endeavour  to  show,  firstly, 
the  association  of  hypertonus  with  sclerosis  ;  secondly,  the 
significance  of  manometer  readings  in  a  number  of  abnormal 
conditions ;  and  how  when  correctly  interpreted  the  records 
are  both  interesting  and  helpful  in  everyday  practice. 


78 


CHAPTER   XI 

THE  CLINICAL  SIGNIFICANCE  AND  VALUE  OF 
HiEMOMANOIVIETER  OBSERVATIONS  IN  AD- 
VANCED INTERSTITIAL  NEPHRITIS 

The  condition  to  which  we  instinctively  turn  in  the  first  place 
for  the  clinical  proof  of  the  accuracy  of  the  contention  as  to 
the  influence  of  the  arterial  wall  in  high  htemomanometer 
readings  is  advanced  interstitial  nephritis.  In  it  the 
vessel  changes,  which  are  very  marked,  are  universally 
recognised.  Such  vessels  as  the  radials  and  temporals,  to 
which  clinical  observation  is  commonly  confined,  are  extra- 
ordinarily thick  and  hard,  and  compared  to  whip-cord.  The 
pulse  in  such  vessels  is,  as  has  been  already  mentioned, 
usually  described  as  a  "  high-tension  pulse,"  as  an  "incom- 
pressible pulse,"  or  as  a  "  hard  pulse."  Medical  literature  is 
full  of  these  terms,  and  there  is  abundant  evidence  available 
to  prove  that  what  was  meant  by  them  was  really  blood- 
pressure.  The  conception  was  that  there  was  peripheral 
resistance,  that  to  overcome  this  the  heart  worked  with 
increased  vigour,  the  consequence  of  which  was  heightened 
pressure  inside  the  vessels,  and  from  this  arose  the  conception 
of  "  high-tension  "  pulses.  Blood-pressure  measuring  instru- 
ments have  been  used  to  illustrate  and  to  support  this  view, 
so  we  propose  to  follow  the  same  method  of  investigation, 
with  a  view  to  ascertaining  the  significance  of  the  records 
these  instruments  give  us. 

As  a  preliminary  to  this  I  present  in  Figs.  29  and  30 
sections  of  the  radial  artery  taken  from  two  cases,  both  fatal, 
from  large  cerebral  haemorrhage.  Fig.  29  was  taken  from  a 
young  man  of  28  years,  who  was  known  to  have  subacute 
interstitial  nephritis,  and  whose  radial  artery  was  thick  and 
hard.      After  a  day  or  two  of  energetic  treatment  for  ureemic 

79 


HtEMOmanometer  observations 

symptoms  the  haemomaiiometer  recorded  a  pressure  of  180 
mm.  Hg.  It  could  not  be  taken  before  treatment  was  begun, 
on  account  of  his  extreme  restlessness.  The  clinical  details 
of  this  case  are  given  at  page  172.  In  the  figure  it  will  be 
noted  that  the  thickening  is  confined  to  the  tunica  media,  and 
that  there  is  no  thickening  of  the  intima. 

Fig.  30  is  the  radial  artery  of  a  man,  aged  50,  brought  into 
my  ward  comatose  and  hemiplegic,  with  the  statement  that  he 
had  been  found  lying  unconscious  beside  his  work.  The  thicken- 
ing of  the  radial  artery  in  this  case  is  much  greater  than  in 
the  preceding  case  ;  but  here  also  the  thickening  is  confined  to 
the  muscular  coat.  Both  cases  therefore  show  in  the  radial 
artery  the  pure  hypertrophy  noted  by  G.  Johnstoue,  Savill, 
and  myself.  Sections  of  the  kidney  from  the  second  case 
showed  a  definite  arterio-sclerotic  atrophy,  in  which  the 
thickening  of  the  intima  predominated  while  the  media  was 
atrophied.  The  changes  corresponded  with  those  represented 
in  Figs.  10  and  12. 

The  pathological  changes  present  in  the  arteries  and 
kidneys  in  cases  of  this  kind  have  been  dealt  with  at  length 
in  Chapter  III.,  and  need  not  be  repeated  here ;  but  for  the 
proper  understanding  of  the  cases  it  is  necessary  to  keep  the 
facts  in  mind.  I  may,  however,  say  that  I  regard  granular 
kidney  as  having  two  modes  of  origin :  one  being  the  result 
of  a  definite  interstitial  nephritis,  the  other  the  result  of 
primary  arterial  changes  such  as  I  have  described.  Pre- 
sumably in  both  forms  changes  corresponding  to  those  I  have 
described  in  the  kidney  occur  also  in  the  brain  vessels. 

It  is  further  to  be  noted  that,  in  the  young  man's  case, 
the  high  reading  of  180  mm.  Hg.  was  obtained  after  active 
measures  had  been  directed  to  the  relaxation  of  his  vessels ; 
below  this  figure  the  pressure  did  not  fall,  for  the  simple 
reason  that  the  thickening  of  his  vessels  could  not  be  further 
removed.  When  the  vessel  wall  was  thicker  the  pressure  was 
doubtless  still  higher.  The  following  four  cases  of  advanced 
interstitial  nephritis  further  illustrate  this  contention. 

Case  6. — A  woman  of  39  years  of  age,  on  admission 
to  the  medical  wards,  had  her  life  saved  by  the  prompt- 
ness of  Dr.  Eousseau,  the  house  physician,  who  withdrew 
about    10    ounces   of    blood    from    the   arm,   when   she   was 

So 


Fig.  29. — The  radial  artery,  showing  liypertrophy  of  tunica  media 
and  no  hypertonic  contraction  (  x  16). 


Fig.  30. — The  radial  artery,  showing  great  hypertrophy  of  the  tunica 
media,  with  slight  hypertonic  contraction  (  x  16). 


INTERSTITIAL  NEPHRITIS 

in  extremis  from  urnemic  dyspnoea  with  acute  engorgement 
of  the  lungs.  She  had  been  under  treatment  on  one  or  two 
occasions  for  some  eye  condition.  On  admission  to  the 
medical  wards  her  condition  was  as  follows.  The  radial 
arteries  were  very  hard  and  thick,  the  heart  was  enlarged  and 
thumping ;  the  urine  contained  albumin,  casts,  and  some  red 
Ijlood  cells.  The  urea  was  4  grains  per  ounce.  There  was 
no  oedema.  In  June  the  hsemomanometer  gave  a  reading  of 
280  to  290  on  the  only  occasion  I  at  that  date  used  the 
instrument  for  her. 

This  patient  was  in  hospital  for  months,  the  rough 
history  of  her  condition  being  that  from  time  to  time  she 
threatened  to  become  ursemic,  and  was  actively  treated  when- 
ever the  symptoms  manifested  themselves.  The  "blood- 
pressure"  taken  on  different  days  and  at  different  hours 
during  September  are  given  below  to  illustrate  the  variations, 
while  some  remarks  are  added. 


Sept 

.  10. 

Forenoon 

5) 

12. 

4.30  p.m. 
9.30     „ 

55 

13. 

1.30  a.m. 
1  p.m. 
3     „ 
7.15  p.m. 

)7 

14. 

Midnight 

)J 

15. 

Noon 

» 

21. 

10  p.m. 

55            55 

J) 

22. 

8.30  p.m. 

55 

23. 

8.30     „ 
11  p.m. 
Midnight 

55 

24. 

8.30  p.m. 

55 

26. 

1  p.m. 

Mm.  Hg. 
(Oliver)     260    Constipated 

,^  _  „  f  Bowels  have  been  freely 
■     ^'"'    (     moved. 
.     255'" 
.     245 

.     260    XotMug  special  to  note 
.     250  '     regarding  her  condi- 
.     255        tion. 
.     245 
.     270j 

rUrremic     since     18th; 
.     265'-      been  treated  by  hot 

(^     pack,  etc. 
.     250    After  hot  pack. 
.     255 
.     255 
.     245 

.     245"jUr8emic  symptoms 

.     230 1     subsided,     condition 
.     240j      much  improved. 


The  pressures  in  this  patient  are  thus  shown  to  have 
varied  between  270  and  230, — below  the  latter  figure 
pressure  did  not  fall.  It  was  noted  in  this  case  that  if  the 
bowels  were  not  moved  the  pressure  rose,  while  after  being 
moved  there  would  be  a  fall,  as  seen  on  the  10th  and  12th, 
when  it  fell  from  260  to  250.  The  effect  of  hot  packs  in 
F  8i 


H^MOMANOMETER  OBSERVATIONS 

reducing  the  pressure  is  also  shown.  When  symptoms  of 
uraemia  began  to  show  themselves  there  was  a  quite  definitely 
palpable  increase  in  the  thickening  of  the  radial  artery  from 
increased  contraction  of  it.  This  is  the  change  commonly 
spoken  of  as  increased  "  tension,"  and  is  thought  of  as  blood- 
pressure,  when  it  ought  to  be  regarded  as  vessel  tightening  up. 
With  this  increase  of  contraction  and  of  consequent  thickening 
the  hsemomanometer  always  gave  a  higher  reading,  while  as 
the  vessel  relaxed  the  reading  fell.  In  this  class  of  case, 
with  a  hypertrophied  and  strongly  acting  heart  and  the 
blood  well  filling  the  vessel,  the  use  of  the  term  "  raised 
tension  "  is  not  unreasonable ;  the  great  drawback  to  it  is 
that  it  has  led  to  the  essential  fact  being  obscured,  for  it 
has  not  been  recognised  that  the  tightening  up  of  the  vessel 
itself  is  the  important  and  essential  part  of  the  phenomena. 
The  measure  of  increase  in  the  intra-arterial  pressure,  which 
is,  of  course,  the  only  true  blood-pressure,  has  been  not  only 
much  overrated,  but  it  does  not  even  necessarily  occur. 

Case  7. — Mr.  S.,  aged  62,  was  sent  to  me  from  the 
North  of  Scotland,  and  his  condition  was  such  that  I  advised 
him  to  go  into  the  Eoyal  Infirmary.  He  was  admitted  on 
the  iOth  September.  He  complained  of  his  eyesight 
having  failed  greatly,  and  on  examination  he  was  found  to 
have  extensive  albuminuric  retinitis.  The  radial  arteries 
were  very  thick  and  hard ;  the  heart  was  enlarged,  and  its 
impulse  forcible.  The  urine  contained  albumin  and  casts. 
He  had  morning  vomiting.  The  hcemomanometer  gave  a 
record  of  260.  After  some  improvement  under  careful 
dieting  and  medicinal  treatment  he  became  steadily  worse,  and 
died  on  the  15th,  five  days  after  admission. 

The  following  observations  were  made  on  this  patient's 
arterial  pressure : — 


Mm.  Hg. 

Sept.  12.  4..30  p.m.  . 

(Oliver)  270  ' 

9.40  „   . 

245 

„   13.  11  a.m. 

220 

1  p.m. 

245 

3\, 

240 

7.15  p.m.  . 

260 

„   14.  Noon 

265 

8  p.m. 

300  + 

„   15  Noon 

295  + 

Died  in  afternoon. 

82 


INTERSTITIAL  NEPHRITIS 

In  this  patient,  while  the  hsemomanometer  gave  pressures 
which  fell  from  270  to  220  as  the  result  of  treatment,  this 
latter  figure  was  the  irreducible  minimum.  The  variations 
in  the  readings  could  be  appreciated  by  the  finger, — the 
radial  definitely  relaxing  as  the  pressure  fell.  The  un- 
favourable course  was  characterised  by  increasing  constriction 
of  the  radials,  and  a  corresponding  rise  in  hsemomanometer 
reading  until  the  heart  failed.  The  changes  in  the  radial  artery 
were  unmistakable  to  the  educated  finger.  The  conclusion 
that  in  the  final  stage  of  this  disease  the  vigour  of  the  heart 
can  rise  to  something  like  200  per  cent,  above  the  normal 
is  unavoidable  if  the  readings  of  our  instruments  are  to  be 
taken  as  representing  Mood-jJresswx.  To  me  the  proposition 
that  with  the  failing  heart  in  this  patient  the  blood-pressure 
was  rising  seems  little  short  of  grotesque.  Whereas  the 
increasing  tightening  up  of  radial  arteries — the  wall  thicken- 
ing and  the  lumen  diminishing — gives  a  reasonable  explanation 
of  the  instrumental  readings  ;  and  these  alterations  were 
unmistakably  to  be  felt  by  the  finger.  They  can  even  be 
seen  when  the  vessel  is  superficial  in  position. 

Case  8. — Mr.  M.,  aged  40,  was  sent  to  see  me  about 
the  middle  of  July  1906.  He  had  only  been  conscious  of  not 
feeling  well  since  about  the  beginning  of  the  year.  It  was 
known  that  he  had  albuminuria,  and  the  question  was 
whether  he  was  to  be  allowed  away  from  home  for  a  holiday. 
When  I  saw  him  the  radial  arteries  were  very  thick  and 
hard ;  the  pulse  was  frequent,  beating  over  100  per 
minute,  while  the  wave  was  small  and  feeble.  The  heart 
was  enlarged,  and  the  first  sound  was  faint.  I  advised  that 
he  should  go  home,  go  to  bed,  and  be  carefully  watched  and 
treated  by  his  medical  attendant.  The  prognosis  I  considered 
was  extremely  gloomy.  After  being  kept  in  bed  till  about 
the  end  of  July,  I  was  asked  to  see  him  again.  He  had 
improved  considerably,  and  I  was  sanguine  that  the  improve- 
ment would  continue  and  make  further  advance.  This 
seems  to  have  been  the  case  for  some  time,  but  he  somewhat 
suddenly  became  worse,  and  died  after  a  convulsive  seizure. 
The  second  time  I  saw  him  the  hEemomanometer  gave  a 
reading  of  250  mm.,  which  was  the  only  observation 
made. 

83 


H^MOMANOMETER  OBSERVATIONS 

This  is  a  type  of  case  one  sees  from  time  to  time  in  the 
consulting-room  and  in  hospital.  They  may  or  may  not  have 
l^een  under  skilled  observation,  symptoms  having  sometimes 
been  disregarded.  In  such  cases  it  will  be  found  that  the 
higher  the  pressure  reading  exceeds  200  the  nearer  is  the 
inevitable  end.  It  means  a  greatly  thickened  artery,  and  a 
tightly  constricted  one, — the  former  a  permanent  anatomical 
thickening,  the  latter  a  hypertonic  contraction.  The  latter 
factor  is  due  to  the  blood,  loaded  with  nitrogenous  w^aste 
products,  so  irritating  the  vessel  wall  as  to  lead  to  its  contrac- 
tion, just  as  we  have  already  seen  that  digitalis  acts. 

In  fact,  in  this  disease  we  have  a  demonstration  of  the 
contention  that  "  waste  products  "  in  the  blood  act  upon  the 
vessels  by  constricting  them.  This  is  a  recognised  fact 
although  there  is  a  curious  hesitancy  in  fully  applying  it. 
However  ignorant  we  may  be  of  the  precise  nature  of  the 
"  waste  products,"  the  state  of  the  kidney  leaves  it  un- 
questioned that  normal  depuration  is  grievously  hindered. 

Case  9.- — Mrs.  M.,  aged  37,  was  admitted  to  the  Eoyal 
Infirmary  on  22nd  September.  The  radial  arteries  were  thick 
and  hard ;  there  was  albuminuria,  and  both  eyes  showed 
marked  albuminuric  retinitis.  The  highest  manometer 
reading  I  have  of  her  artery  is  235  mm.  Hg.  She  stayed  in 
hospital  for  a  few  days  only,  as  she  wanted  to  return  to 
her  family. 

The  following  observations  were  made  in  this  patient : — 

Mm.  Hg. 
Sept.  22.     8.30  p.m.  .  .      (Oliver)  220 

„      23.     8.25     „     .  .  .         230 

"    ■  ■  "  \     had  acted  freely. 

Midiiiglit .  .  .        205 

„      24.     8.30  p.m.  .  .  .210 

„      26.     1       „       .  .  .         235 

In  the  preceding  three  cases  in  which  a  number  of 
observations  were  made,  the  readings  varied  in 

Case  6      .  .  .      from  230  to  270  mm.  Hg. 

Case  7      .  .  .         „      270  to  300+     do. 

Case  9      .  .  .         „     200  to  235         do. 

while  in  Case  8,  with  one  observation  it  was  260  do, 

84 


INTERSTITIAL  NEPHRITIS 

If  the  normal  be  taken  as  100  to  120 — the  precise 
figure  not  being  of  much  importance  for  our  present  purpose 
— we  have  here  four  cases  with  an  increase  of  from  100  per 
cent,  upwards — two,  two  and  a  half  times,  almost  three 
times  the  normal.  And  we  are  asked  to  accept  this  as 
"  blood-pressure  "  !  The  claim,  if  it  means  anything,  is  this, — 
owing  to  conditions  in  the  blood  the  peripheral  resistance  is 
increased,  and  the  heart,  responding  to  the  call  for  more  work, 
increases  in  power  so  as  to  cope  with  the  resistance,  and 
develops  a  power  which  gives  even  in  the  brachial  artery  a 
pressure  from  say  twice  to  two  and  a  half  times  more  than 
the  normal.  With  the  fullest  appreciation  of  the  reserve 
power  in  the  heart  we  cannot  but  think  there  is  a  big  error 
here.  Taking  Case  6  as  the  case  in  which  the  greatest 
number  of  observations  were  made,  it  is  seen  that  the  readings 
ranged  from  230  to  270,  a  margin  of  40,  but  below  this  it 
never  fell ;  in  Case  2  it  never  fell  below  220;  and  in  Case 
3  never  below  200.  The  lower  figures  were  in  some 
instances  the  direct  result  of  treatment,  but  no  kind  of  treat- 
ment reduced  them  further, — this  apparently  was  the 
irreducible  minimum.  In  all  four  cases  the  disease  was  the 
same,  and  in  all  there  was  great  and  permanent  thickening 
of  the  arterial  walls.  Now  what  is  done  by  such  instru- 
ments as  we  use  is  this — the  pressure  in  them  is  raised 
until  the  arterial  circulation  is  arrested  in  the  part ;  this 
means  that  the  artery  is  so  compressed  by  the  pressure  of  the 
surrounding  soft  tissues  that  its  lumen  is  obliterated.  The 
result  depends,  therefore,  upon  the  compressibility  of  the 
artery,  and  the  compressibility  of  a  tube,  as  has  been  already 
shown,  depends  upon  the  thickness  of  its  wall.  The  question 
has  been  dealt  with  from  the  purely  physical  side,  and  it  is 
seen  that  the  clinical  facts,  in  the  condition  dealt  with  in 
this  chapter,  are  in  complete  harmony  with  them,  and  indeed 
with  common  knowledge  as  well. 

In  our  four  cases  there  was  no  doubt  about  the  great 
thickening  of  the  arteries ;  and  this  must  be  regarded  as 
having  been  a  large  factor  in  determining  the  high  mano- 
meter readings.  The  degree  of  thickness  of  the  arterial  wall 
becomes  therefore  a  factor  of  high  value  in  determining  the 
height  of  heemomanometer  readings.      The  cases  gave  further 

85 


H.EMOMANOMETER  OBSERVATIONS 

proof  of  the  accuracy  of  this.  It  was  quite  unniistakably 
observed  by  the  finger  that  when  the  manometer  readings  fell 
the  radial  artery  became  slightly  softer  and  larger.  This  was 
corroborated  by  others,  for  when  attention  was  directed  to 
the  changes  in  the  radial  artery  I  found  that  my  assistants 
and  others  soon  acquired  the  faculty  of  recognising  the 
changes,  and  soon  became  much  interested  in  their  observa- 
tion. On  the  other  hand,  when  the  vessel  tightened  up  the 
manometer  reading  rose.  The  relaxation  of  the  radials  soon 
after  the  administration  of  erythrol  I  have  demonstrated  to  a 
class  of  graduates,  and  shown  that  it  corresponded  with  a  fall 
in  manometer  reading.  In  the  same  way  a  hot  pack  relaxes 
the  radial  artery  so  as  to  be  apparent  to  the  sense  of  touch, 
while  the  manometer  reading  was  reduced ;  so  also,  after 
purgation  or  free  bowel  movement,  there  was  relaxation  and 
lowered  reading.  Instead  of  recognising  and  watching  the 
vessel  changes  in  this  disease,  clinicians  have  thought  only 
of  the  blood-pressure  in  the  radial  artery ;  and  I  do  not 
doubt  that  the  increased  thickening  or  hardening  of  wall  was 
usually  called  tension,  and  thought  of  as  blood-pressure. 

The  determination  of  how  much  is  blood-pressure,  and 
how  much  is  to  be  attributed  to  the  increased  thickness  in 
the  vessel  wall,  does  not  seem  to  me  to  be  capable  of  instru- 
mental proof.  The  lowest  record  in  these  four  cases  was  200 
mm.  Hg.  and  no  matter  what  measures  were  taken  this  great 
heightening  in  the  readings  persisted,  just  as  the  thickening  of 
the  arterial  wall  persisted,  and  to  which  I  contend  it  was  due. 
The  readings,  however,  rose  and  fell.  In  Case  6  a  pressure  of 
230  would  rise  to  270,  a  rise  of  40  mm.  Hg.,  a  greater  rise 
than  the  physiologists  tell  us  takes  place  after  violent  exertion  ; 
and  we  are  asked  to  believe  that  a  heart  already  doing  100  per 
cent,  more  work  than  normal  finds  no  difficulty  in  doing  this 
extra  40  mm.  Hg.  In  Case  7  the  pressure  rose  to  over  300 
mm.  Hg.  when  the  patient  was  dying  and  the  heart  giving 
out.  I  submit  that  when  these  rises  occur  the  radial  artery 
contracts,  that  as  a  consequence  its  wall  still  further  thickens 
and  its  lumen  diminishes ;  and,  seeing  that  the  arterial  wall 
takes  a  large  share  in  giving  the  high  manometer  readings, 
this  hypertonic  contraction  of  the  sclerosed  vessel  explains 
the  further  increase  in  the  manometer  reading.      The  hyper- 

86 


INTERSTITIAL  NEPHRITIS 

tonic  contraction,  as  I  have  already  said,  can  be  followed  by 
the  finger,  so  that  there  is  no  doubt  whatever  as  to  its  taking 
place.  What  the  blood-pressure  is  inside  that  tighten ed-up 
artery  is  a  totally  different  problem,  and  one  which  can  only 
be  dealt  with  and  investigated  indirectly.  I  submit  that  the 
readings  do  not  represent  blood-pressure.  That  the  state 
of  the  arterial  wall  is  sufficient  to  explain  them  is  probably 
not  far  from  the  precise  truth.  In  fact,  my  belief  is  that  not 
only  in  chronic  kidney  disease,  but  in  all  disorders,  the  arterial 
wall  has  to  be  given  a  prominent  place  when  htemomanometer 
readings  are  interpreted.  That  being  so,  vessel  thickening, 
whenever  present,  takes  from  hffimomanometer  readings  the 
value  which  has  been  attributed  to  them  as  records  of  real 
blood-pressure. 

At  the  same  time,  it  must  be  equally  insisted  upon  that 
these  records  are  of  interest  and  of  value,  and  are  not  to  be 
put  aside  as  worthless, — the  fate  which  has  befallen  them  at 
the  hands  of  not  a  few  very  able  and  critical  physicians. 

With  arteries  such  as  are  invariably  met  with  in 
advanced  interstitial  nephritis  high  readings  will  always  be 
got ;  but,  as  has  been  shown  in  the  preceding  cases,  there  is 
a  wide  range  of  movement  in  the  readings,  according  to  the 
condition  of  the  patient,  although  the  high  level  is  always 
maintained.  This  range  indicates  the  margin  within  which 
remedies  act,  and  the  effect  of  these  will  be  found  to  be  use- 
fully defined  and  represented  by  the  readings.  Had  I  to 
make  the  choice  I  would  select  to  have  my  fingers  rather 
than  the  haemomanometer ;  but  I  am  glad  to  have  both,  for 
the  instrument  gives  me  a  record  of  numbers  which  I  can  pre- 
sent to  others,  while  the  skill  of  my  fingers  belongs  entirely 
to  myself,  and  cannot  be  transferred  to  a  chart.  The  instru- 
ment, in  such  cases  as  those  recorded,  gives  a  minute  record 
from  hour  to  hour,  and  day  to  day,  of  the  state  of  the  arteries  ; 
and  as  my  contention  is  that  the  varying  degree  of  arterial 
contraction  depends  upon  the  condition  of  the  blood,  the 
readings  indicate  that  condition,  and  they  thus  become  an 
invaluable  guide  to  treatment,  and  to  the  daily  management 
of  these  critical  cases.  It  is  desirable,  however,  to  accentuate 
the  point  that  a  high  pressure  is  not  necessarily  an  indication 
that  relaxing  and  reducing  treatment  is  to  be  adopted.      In 

87 


H.EMOMANOMETER  OBSERVATIONS 

Case  9  a  pressure  of  235  could  stand  active  measures  for 
reduction ;  in  Case  6,  with  the  pressure  reduced  to  230,  it 
would  have  been  unsafe  to  have  continued  the  relaxing 
treatment  longer ;  while  in  Case  7  I  was  not  satisfied  that 
the  pressure,  when  lowered  to  220,  had  not  somewhat 
overstepped  the  safe  limit.  It  is  here  the  skill  of  the  physi- 
cian's finger  comes  in, — it  is  by  that  means  that  the  wave 
inside  the  hard  vessel  is  estimated,  and  no  instrument  can 
do  this  for  ns,  nor,  I  venture  to  predict,  will  an  instrument 
ever  be  devised  to  replace  the  tactus  eruclihis. 


88 


CHAPTER   XII 

THE  INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 
IN  CAUSING  ARTERIAL  HYPERTONUS  AND 
SCLEROSIS  :  FOOD,  DIGESTION,  CONSTIPATION, 
AND  ALCOHOL. 

THE    IXFLUEXCE    OF    DIET    ON    SCLEEOSED    VESSELS. 
THE    INTLUEXCE    OF    DIET    ON    THE    ADEENALS. 

It  has  been  long  and  fully  recognised  that  certain  conditions 
having  their  origin  in  the  alimentary  tract  were  accompanied 
by  changes  in  the  pulse.  The  changes  have  come  to  be 
generally  referred  to  as  alterations  in  blood-pressure ;  altera- 
tions which  modified  or  changed  the  relation  between  the 
vessel  wall  and  the  circulating  blood  within  it.  The  terms 
in  common  use  to  define  the  change  have  been  "  incompres- 
sibility  "  and  "  tension  "  :  terms  indicating  either  the  conception 
formed  of  the  strength  or  force  of  the  stream,  or  the  state  of  the 
vessel  wall  as  determined  by  the  blood  inside  it.  That  these 
terms  have  come  to  be  very  inaccurately  used  by  many 
practitioners  will  not  be  disputed.  Controversy  has  taken 
place  as  to  the  meaning  of  the  word  "  tension,"  and,  so  far  as 
I  am  able  to  judge,  the  word  as  used  in  clinical  medicine  has 
not  the  same  significance  as  it  has  to  the  pure  physicist.  The 
word  has  been  borrowed  from  physics,  where  it  has  a  very 
wide  significance,  and  applied  in  clinical  medicine  to  indicate 
one  set  of  phenomena.  To  the  purist  the  use  of  the  word  in 
medicine  tends  therefore  to  be  either  an  offence  or  a  stumbling- 
block.  It  seems  to  me  that  in  clinical  medicine  it  is  used  to 
express  the  mechanical  effect  of  the  circulating  blood  and  the 
pulse  wave  upon  the  vessel  wall  as  it  can  be  estimated  by  the 
educated  finger.      The  effect  depends  of  course  upon  the  ful- 

89 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

ness  of  the  vessel.  If  the  vessel  continues  well  filled  during 
diastole,  the  wave  which  travels  along  it  with  each  cardiac 
systole  gives  to  the  finger  the  feeling  of  greater  fulness,  with 
a  sense  of  obstruction  in  the  vessel  wall  to  the  stretching. 

It  is  these  two  factors  which  are  comprised  in  the  word 
"  tension  "  as  intelligently  interpreted.  The  feeling  of  greater 
fulness,  which  may  be  present  even  during  diastole,  is  produced 
in  the  radial  artery  in  two  ways — namely,  by  a  constriction  of 
the  vessels  on  the  distal  side  of  the  wrist,  or  by  a  contraction 
of  the  radial  artery  itself. 

This  sense  of  increased  fulness  is  due  in  the  first  of  these 
to   a   local   increase  in  the  amount   of  blood   in   the  vessel 
and  to   a  local  rise   of   blood-pressure  in   the   radial  artery. 
No  change  in  the  action  of  the  heart  is  necessary  for  the 
production  of  this  effect ;  it  is  the  hievitable  effect,  and  it  is  a 
purely  physical  phenomenon.      It  can  be  felt  in  the  radial 
artery    by    keeping    one    finger    on    it    when    the   vessel    is 
obliterated    by   another  placed    on    the    distal    side    of    the 
point  selected.      It  can  also    be   shown   by  compressing  the 
superjicialis    voice   branch    while    a    finger    is   on    the   radial 
at  the  wrist.      In  both   these   simple   procedures   the  radial 
artery  is  felt   to  become   fuller   and   therefore    tenser.      The 
same  feeling  of  fulness  may  be  produced  by  the  radial  artery 
participating,  as  it  commonly  does,  in  capillary  contraction. 
The  contraction  thickens  the  arterial  wall  and  brings  it  into 
a   different  relation  to  its    contained   blood.      As  Broadbent 
long  ago  pointed  out,  the   normal  artery  during  diastole  is 
oval  when  viewed  in  transverse  section,  while  the  passage  of 
the  pulse  wave  alters  the  oval  to  a  round.      When  an  artery 
is  hypertonically  contracted  it  changes  from  the  oval  towards 
the  round,  until  with   sufficient    thickness  it  maintains  the 
round  outline.      It  follows  that  when  the  pulse  wave  passes 
along  the  hypertonic  artery  it  gives  through  the  finger  a  sense 
of  greater  resistance.      I  venture  to  believe  that  this  was  the 
"  heightened  tension  "  of  our  best  clinicians.      That  confusion 
should  have  arisen  between  clinical  observation  and  physio- 
logical   teaching   was    inevitable.      To    the    initiated,    tension 
meant  this  relation  between  the  blood  and  the  vessel  wall ; 
and  it  was  the  true  appreciation  of  this  relation  which  re- 
vealed the  tactus  eruditus  of  the  physician. 

90 


FOOD,  DIGESTION,  CONSTIPATION,  AND  ALCOHOL 

The  idea  of  "  fulness  "  in  an  artery  is  thus  easy  of  inter- 
pretation, and  is  used  in  quite  a  sound  sense  ;  but  it  has  given 
rise  to  another  conception — namely,  that  there  is  an  increased 
volume  of  blood — not  a  local  but  a  general  increase.  This 
is  not  by  any  means  so  sound  a  view,  although  common 
enough ;  and  it  is  one  of  the  views  which  has  shared  not 
a  little  in  hindering  a  more  correct  understanding  of  the 
phenomena  presented  by  the  circulation  in  a  great  variety  of 
general  disorders.  The  idea  of  increased  volume  of  blood  is 
of  course  the  "  plethora  "  of  the  past  century,  not  to  go  farther 
back ;  while  the  idea  of  "  depletion "  as  the  remedy  for 
"plethora"  has  survived,  although  transferred  from  blood- 
letting to  purgation. 

This  fulness  of  blood,  or  full-bloodedness,  was  commonly 
associated  with  the  idea  of  high,  or  large,  feeding,  and  the 
free  use  of  alcoholic  liquors.  It  naturally  enough  was 
literally  interpreted  as  the  result  of  a  too  abundant  supply  of 
nutriment  added  to  the  blood.  This  type  was  seen  in  the  per- 
son of  florid  face,  bulky  frame,  and  full,  strong,  and  hard  pulse. 
The  effect  of  the  condition  of  the  alimentary  tract  upon 
the  pulse  was,  however,  also  recognised  in  another  type.  The 
individual  in  this  class  did  not  so  plainly  show  that  he  in- 
dulged to  excess,  but  yet  he  too  suffered  from  attacks  of 
"  biliousness  "  or  of  "  disordered  liver."  In  him  also  the  pulse 
was  of  "  high  tension  " — it  was  harder,  firmer,  and  less  com- 
pressible. 

It  is  indeed  evident  that  a  relationship  between  the 
alimentary  tract  and  the  circulation  has  been  long  recognised 
in  medicine.  The  association  of  the  two  is  no  novel  doctrine, 
for  it  forms  now  and  has  formed  for  generations  the  basis  of 
treatment.  The  treatment  has  consisted  of  free  unloadino; 
of  the  alimentary  tract,  and  a  reduction  in  the  amount  of  and 
often  an  alteration  in  the  kind  of  food  and  fluid  usually  taken. 
The  result  was  the  relief  of  the  patient's  symptoms,  w^hile  the 
reduction  of  pulse  tension  gave  countenance  to  the  idea  of 
depletion. 

This  is  the  common  knowledge  of  the  profession,  yet  to 
get  the  full  meaning  and  the  full  value  out  of  this  common- 
place belief  and  proceeding,  it  is  necessary  to  examine  the 
matter  more  fully. 

91 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

We  may  assume  that  it  is  generally  accepted  that  generous 
feeding  and  the  free  use  of  alcoholic  and  malt  liquors  lead  to 
the  condition  of  pulse  which  is  called  "  high  tension,"  especially 
if  there  be  not  daily,  full,  and  free  evacuation  of  intestinal 
contents.  This  is  the  gross  type,  and  I  think  it  is  more 
common  in  some  parts  of  this  island  than  in  others ;  and  it 
occurs  without  doubt  more  commonly  in  some  classes  than  in 
others.  The  individual  of  this  type  often  dies  in  com- 
paratively early  life  as  a  result  of  vascular  changes  in  brain 
and  kidneys.  This  gross  type  is  readily  accepted  with  all 
its  clinical  and  pathological  significance.  It  is  accepted 
that  liberal  feeding  and  drinking  lead  to  "raised  arterial 
tension,"  to  permanent  vascular  changes,  and  to  early  death 
the  result  of  these.  While  this  is  the  case,  there  is  by  no 
means  the  same  frank  recognition  that  there  are  necessarily 
minor  degrees  of  the  same  class  of  phenomena,  and  that  the 
minor  degrees  can  produce  similar  results  although  taking  a 
longer  time  to  effect  them. 

I  take  it  that  it  was  the  gross  type  that  determined  the 
idea  of  plethora,  and  its  treatment  by  depletion ;  and  that 
this  has  prevented  the  learning  of  the  lessons  which  the  lesser 
degrees  were  capable  of  teaching.  In  the  gross  type  the  idea 
was  a  heightened  tension  from  over-filling — the  vessels  were 
too  full,  and  the  consequent  pressure  upon  their  walls  increased 
the  risk  of  rupture. 

The  more  modern  mode  of  expression  is  that  "  high 
tension  "  is  due  to  "  peripheral  resistance,"  and  yet  this  peri- 
pheral resistance  seems  to  have  an  elusive  existence  when  an 
attempt  is  made  to  come  to  close  quarters  with  it.  I  do  not 
question  its  recognition  by  some,  but  there  seems  to  be  often 
a  vagueness  about  it  which  is  most  undesirable  on  such  a 
very  practical  matter,  and  indicates  a  want  of  clear  thinking 
which  is  equally  undesirable. 

There  is  no  one  more  entitled  to  define  the  position  than 
Sir  William  Broadbent,  who  rightly  ranked  as  one  of  our 
greatest  clinicians.  He  regarded  capillary  resistance  as  the 
cause  of  high  tension ;  and  amongst  the  causes  of  capillary 
resistance  he  included  nitrogenous  waste,  and  the  products  of 
imperfect  metabolism.  He  also  knew  that  capillary  resist- 
ance might  be  due  to  contraction   of  the  capillaries.      This 

92 


FOOD,  DIGESTION,  CONSTIPATION,  AND  ALCOHOL 

seems  to  me  to  be  as  far  as  he  got.  The  term  tension  seems 
to  have  satisfied  clinicians,  and  therefore  to  have  lulled 
inquiry ;  the  introduction  of  the  term  liypertension  is  the 
latest  corroboration  of  this  suggestion. 

It  seems  to  me  that  the  idea  of  "  tension "  has  so 
dominated  clinical  medicine  that  the  great  and  fundamental 
fact  in  the  phenomena — namely,  the  fact  of  arterial  contraction 
as  it  occurs  in  the  radial  and  other  arteries — has  been  entirely 
overlooked.  This  contraction,  which  I  have  called  hypertonic 
contraction,  has  been  considered  in  Chapters  I.  and  IV.,  and 
it  is  unnecessary  to  repeat  what  has  already  been  written. 
Here  it  is  only  necessary  to  emphasise  the  fact  that  the 
"  hio-h  tension "  of  the  "  bilious  attack,"  of  the  "  disordered 
liver,"  of  constipation,  is  determined  by  vessel  constriction, 
and  that  that  constriction  is  in  the  systemic  arteries. 
That  the  capillaries  are  contracted  also  is  certain,  but 
whether  as  part  of  the  initial  contraction,  or  as  merely 
secondary  to  arterial  contraction,  it  is  difficult  to  determine 
with  certainty.  At  the  same  time,  I  distinctly  lean  to  the 
view  that  the  initial  contraction  affects  both  capillaries  and 
arteries,  my  grounds  for  the  opinion  being  the  conviction  that 
in  some  at  least  of  the  gastro-intestinal  conditions  which  lead 
to  "high  tension,"  the  vessel  contraction  is  caused  by  the 
dkect  influence  on  the  vessel  wall  of  substances  absorbed 
from  the  intestine,  acting  as  digitalis,  ergot,  and  adrenalin 
act,  and  that  the  capillaries  cannot  be  excluded  from  such 
influences  or  from  such  action. 

The  question  of  the  precise  relations  of  the  ahmentary 
conditions,  which  are  the  primary  cause  of  the  vessel  pheno- 
mena, is  somewhat  complex  and  requires  detailed  examination. 
During  the  process  of  digestion  there  is  a  normal  reflex, 
acting  from  the  splanchnic  area  through  the  vasomotor  centre 
in  the  medulla,  which  leads  to  systemic  arterial  contraction. 
This,  however,  is  only  one  aspect  of  the  influence  of  the 
alimentary  system  upon  the  blood-vessels ;  the  further  effect 
may  be  produced  by  two  factors — namely,  the  absorption  of  an 
excess  of  the  nutritive  products  of  digestion,  or  the  absorption 
of  the  products  of  intestinal  putrefaction. 

Taking  the   first   of  these   two   causes,  it  is  not  open  to 
question  that  the  big  feeder  presents  the  phenomena  already 

9^ 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

indicated.  He  eats  more  than  his  tissues  require  for  repairing 
loss  or  maintaining  energy,  and,  if  he  has  a  vigorous  digestion, 
the  conversion  of  his  food  into  suitable  nutritive  pabulum  is 
equally  in  excess,  and  his  blood  becomes  surcharged  with 
materials  which  cannot  be  utilised,  which  have  to  be  dis- 
integrated to  make  their  removal  possible.  This  extra  work 
interferes  with  the  metabolic  processes  necessary  for  the 
removal  of  the  normal  waste  of  tissue.  In  this  way  are 
supplied  tbe  "  nitrogenous  waste  and  the  products  of  imper- 
fect metabolism"  which  lead  to  the  "  bihous  attack"  with 
its  vessel  contraction  and  high  blood-pressure. 

The  second  factor  to  be  dealt  with  is  the  absorption  of 
putrefactive  products  from  the  intestine. 

In  the  case  of  animal  food,  which  embraces  flesh  of  all 
kinds  and  eggs,  it  will  be  found  that  its  retention  in  the 
intestinal  tract  leads  to  putrefactive  changes.  This  putre- 
faction is  brought  about  by  the  bacilli  belonging  to  the  colon 
group,  which  are  the  normal  occupants  of  this  tract.  The 
process  of  putrefaction  occurs  most  readily  in  the  organic 
compounds  present  in  animal  albumin.  In  fact,  for  clinical 
and  practical  purposes,  intestinal  putrefaction  may  be  regarded 
as  always  due  to  the  decomposition  of  animal  food.  There  is 
an  important  exception  to  this — namely,  milk.  This  putre- 
factive decomposition  of  animal  organic  substances  occurs  in 
constipation,  and,  of  course,  the  necessary  sequence  is  that 
constipation  being  present,  the  products  of  decomposition  are 
not  got  rid  of  by  the  bowel,  or  are  only  got  rid  of  in  direct 
ratio  to  the  measure  of  intestinal  evacuation.  Constipation 
thus  leads  not  only  to  putrefaction,  but  to  the  retention  in, 
or  absorption  from,  the  intestines  of  the  products  produced 
during  putrefaction.  In  the  breaking  up  or  cleavage  of  the 
proteid  molecule  in  the  putrefactive  process,  a  number  of 
substances  are  produced,  and  are  absorbed  from  the  intestine. 
Some  of  these  substances  are  known  to  have  a  toxic  and 
injurious  effect  upon  the  body.  They  all  belong  to  what  is 
technically  known  as  the  aromatic  series.  The  best  known 
of  them  are  skatol,  indol,  and  phenol.  These  aromatic 
products  of  intestinal  putrefaction  reach  the  liver,  where 
they  combine  with  sulphuric  acid  and  are  excreted  in  the 
urine  as  ethereal  sulphates.      The  presence  of   an  excess  of 

94 


FOOD,  DIGESTION,  CONSTIPATION,  AND  ALCOHOL 

ethereal  sulphates  in  the  urine  becomes  thus  the  measure  and 
gauge  of  the  degree  of  intestinal  putrefaction  present.  The 
measure  of  indican  in  the  urine  has  the  same  significance. 
The  indol  is  rapidly  absorbed  from  the  intestinal  tract  and 
carried  by  the  portal  blood  to  the  liver,  where  it  enters  into 
loose  combination  with  the  liver  cells.  From  this  combina- 
tion it  is  readily  detached,  to  become  imited  with  sulphuric 
acid.  Before  becoming  thus  united,  it  becomes  oxidised 
into  indoxyl,  so  that  when  united  it  becomes  chemically  a 
potassium  salt  known  as  indoxyl  sulphate  of  potassium. 
This  substance  is  much  less  toxic  than  indol,  finds  its  way 
into  the  blood,  and  is  promptly  excreted  in  the  urine  and 
known  as  indican. 

In  regard  to  the  toxic  properties  of  the  substances 
referred  to,  there  appears  to  be  abundant  room  for  further 
investigation  into  their  action.  The  difficulties  attending 
such  investigations  are  necessarily  very  great,  for  it  is  to  be 
remembered  that  in  the  human  subject — and  it  is  in  relation 
to  practical  medicine  that  these  cjuestions  really  interest  us — 
the  toxaemia  is  often  a  slow  and  long-continued  condition,  the- 
very  slowness  of  which  is  apt  to  arouse  scepticism  in  the 
minds  of  those  who  have  not  looked  into  the  more  subtle 
processes  carried  on  in  the  animal  body.  Such  an  authority 
as  Herter  is  satisfied  of  the  toxic  properties  possessed  by 
indol ;  that,  in  addition  to  its  power  to  produce  evanescent 
conditions  as  headache,  irritability,  and  restlessness,  it  can,  by 
its  prolonged  absorption,  contribute  to  the  production  of 
chronic  nervous  disorder. 

It  may  be  asked,  how  do  these  effects  compare  with 
effects  following  upon  analogous  processes  in  carbohydrate 
food  ?  And  the  answer  is  that  while  the  fermentative  pro- 
cesses which  occur  in  them  may  lead  to  impleasant  symptoms, 
yet  the  substances  produced  are  by  no  means  so  toxic  or  so 
injurious  as  those  produced  during  proteid  putrefaction. 

While  constipation  is  such  an  important  factor  in  favouring 
putrefactive  changes  in  the  proteid  contents  of  the  intestine, 
it  is  necessary  to  state  that  other  factors  operate  or  co-operate 
in  favouring  these :  defects  in  proteid  digestion,  due  to  dis- 
order of  gastric  or  pancreatic  function,  may  lead  to  very 
imperfect    and    incomplete    changes     in    the     proteid     food 

95 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

taken,  and  such  incomplete  transformation  favours  the 
onset  of  putrefactive  changes.  A  furtlier  important  side 
to  this  question  is  that  a  diet,  very  rich  in  proteid,  may 
be  thoroughly  digested,  may  be  thoroughly  converted  into 
albumoses  and  peptones  and  ready  for  intestinal  absorption, 
but  the  absorption  may  be  prevented  or  delayed  in  conse- 
quence of  their  quantity  or  abundance  in  the  intestine. 
This  delay  in  absorption  is  fatal  to  those  highly  evolved 
products,  for  the  organisms  which  produce  putrefaction  find 
in  them  material  on  which  they  act  with  great  facility. 
There  is  thus  a  considerable  variety  in  the  conditions  under 
which  intestinal  putrefaction  occurs.  In  all  there  is  the 
common  factor  of  absorption  of  the  products  of  putrefaction. 

When  there  is  this  absorption  of  -pntref action  products  from 
the  intestinal  tract,  there  is,  in  the  great  majority  of  cases, 
the  vessel  contrctction  with  ichich  toe  are  dealing — this  is  the 
main  objective  evidence  supplied  by  the  examination  of  the 
circulatory  system,  and,  when  present,  the  hiTemomanometer 
reading  is  high,  that  is  to  say,  high  as  compared  with  what 
it  records  when  the  condition  is  removed  and  the  vessel 
contraction  relaxed. 

The  symptoms  and  degree  of  discomfort  caused  by  the 
absorption  of  the  substances  referred  to  varies  within 
extraordinarily  wide  limits.  Some  persons  are  remarkably 
sensitive  to  the  toxins  under  consideration.  Old  people  are 
more  sensitive  than  young  or  middle-aged  people.  It  might 
naturally  be  assumed  that  individuals  of  the  definitely  nervous 
type  would  always  suffer  most,  and  that  the  labouring  class 
would  be  but  little  susceptible  to  them.  While  this  assump- 
tion cannot  be  altogether  set  aside  as  incorrect,  I  am  often 
surprised  to  find  amongst  the  out-patients  coming  to  me  at  the 
Eoyal  Infirmary  individuals  of  the  labouring  class  suffering 
so  profoundly  from  intestinal  auto-intoxication  as  to  be  unfit 
for  work.  In  some  persons  the  manifestations  of  intoxication 
are  so  pronounced  that  they  indicate  a  definite  idiosyncrasy, 
an  individual  chemico-vital  susceptibility,  which  is  not,  so  far 
as  can  be  seen,  a  matter  determined  by  social  class  distinctions 
or  by  occupation. 

The  question  that  emerges  from  the  relations  here 
submitted  as  subsisting  between  alimentation,  the  fate  of  food 

96 


FOOD,  DIGESTION,  CONSTIPATION,  AND  ALCOHOL 

in  the  alimentary  tract,  and  the  effect  upon  the  composition 
of  the  blood  of  absorption  from  that  tract  is :  How  much  is 
the  effect  upon  the  vessels  to  be  attributed  to  the  normal 
reflex  acting  through  the  vasomotor  centre  in  the  medulla, 
and  how  much  to  the  direct  influence  on  the  vessels  of 
substances  present  in  the  blood  ?  Which,  for  instance,  of 
these  is  the  main  and  leading  factor  in  constipation  ?  Does 
the  retention  of  excrement  in  the  intestine  continue  so  to 
stimulate  the-  splanchnic  system  that  the  stimulation  of  the 
centre  for  vasomotor  constriction  is  continuously  maintained  ; 
or,  on  the  other  hand,  does  the  continuous  absorption  into 
and  therefore  the  presence  of  noxious  substances  in  the 
blood  bring  these  substances  into  direct  contact  with  the 
vessel  wall,  stimulating  or  exciting  it  to  a  hypertonic  contrac- 
tion ?  It  is  probable  that  both  factors  operate.  There  is  no 
doubt  as  to  the  nervous  reflex,  and  there  is  little  doubt  as  to 
the  other  factor.  It  has  been  already  shown  that  certain 
substances  added  to  the  blood  lead  to  vessel  contraction 
without  the  aid  of  the  nervous  system.  It  is  of  course 
always  interesting  to  know  the  precise  steps  by  which  effects 
which  interest  us  are  obtained ;  but  it  remains  to  be  settled 
whether  the  substances  to  which  we  refer  and  which  cause 
vessel  constriction  act  through  the  nervous  apparatus  or  more 
immediately  upon  the  muscle  tissue  of  the  vessel  wall. 
Even  in  this  connection  it  is,  however,  to  be  borne  in  mind 
that  when  there  exists  a  complex  nervous  mechanism  it 
becomes  involved  in  processes,  although  a  like  result  can  be 
obtained  without  its  participation.  This  is  shown  by  the 
fact  referred  to  earlier  that  the  tone  of  arteries  is  soon 
restored  after  section  of  vasomotor  nerves.  I  do  not  claim 
that  the  substances  which  act  as  it  is  here  held  they  do,  have 
been  individually  and  severally  separated  and  investigated  ;  and 
yet  I  do  not  think  any  physician  of  experience  questions  the 
correctness  of  the  general  belief  in  "  blood  impurity,"  and 
that  it  commonly  has  its  rise  in  disorder  of  the  alimentary 
system,  or  is  brought  about,  directly  or  indirectly,  by  absorption 
from  that  tract.  The  muddy  complexion,  the  "  dirty " 
conjunctiva,  the  face  pimples,  are  the  visible  manifestations 
of  the  accuracy  of  the  popular  conception.  That  the  blood - 
content  is  influenced  by  what  is  taken  into  the  alimentary 
G  97 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

system  has  much  support  from  the  common  knowledge  as 
to  the  production  of  urticaria  by  the  ingestion  of  certain 
substances  by  certain  persons.  The  extreme  subtlety  of 
blood-content  is  realised  when  a  little  shell-fish  in  one  person, 
a  few  gooseberries  or  strawberries  in  another,  will  lead  to  an 
extensive  urticaria  which  is  only  to  be  explained  by  the 
action  of  something  brought  to  the  surface  by  the  blood. 
Although  the  something  has  not  been  separated  and  christened, 
it  would  be  the  merest  scientific  priggery  to  question  its 
existence  or  to  deny  the  sequence  of  phenomena.  That 
deleterious  substances  enter  the  blood  from  the  intestinal 
tract  cannot  be  seriously  questioned,  and  believing  this,  it  is 
not  necessary  to  occupy  space  in  further  argument  in  support 
of  its  truth.  The  acceptance  of  this  carries  the  acceptance 
of  the  minor  truth,  that  the  amount  or  quantity  of  such 
deleterious  substances  varies  within  very  wide  limits,  and 
that  whatever  effect  they  may  have  will  equally  vary  in 
degree. 

The  fact  on  which  I  seek  to  lay  great  emphasis  is  that 
substances  absorbed  from  the  alimentary  tract  lead  to  vessel 
contraction.  That  fact  seems  to  me  to  be  fundamental  and 
not  open  to  question.  To  my  mind  it  seems  unreasonable  to 
suppose  that  such  substances  cause  vessel  constriction  only 
through  the  systemic  vasomotor  centre.  It  has  been  seen 
how  erroneous  is  the  common  tendency  to  attribute  all  such 
vascular  changes  to  that  mechanism,  and  that  experimental 
investigation  has  proved  that  even  substances  which  belong 
to  our  most  important  medicinal  remedies  act  not  through 
that  mechanism  but  directly  upon  the  vessel  wall.  I  contend 
further  that  clinical  indications  point  to  this  direct  influence 
on  the  vessel  wall  of  substances  absorbed  from  the  intestinal 
tract,  and  that  the  common  effect  is  a  hypertonic  contraction 
of  the  arteries.  It  is  this  arterial  contraction  which  has  not 
been  recognised  as  the  essential  factor  in  the  production  of 
the  "  high  tension  "  associated  with  certain  conditions  in  the 
alimentary  system,  and  which  has  been  so  much  written 
about.  I  have  failed  to  find  any  indication  that  the  steps  by 
which  the  "  high  tension  "  was  brought  about  ever  got  beyond 
the  nebulous  idea  of  "  peripheral  resistance." 

My  contention   at   this   stage   may  be   thus  stated :  as  a 

98' 


FOOD,  DIGESTION,  CONSTIPATION,  AND  ALCOHOL 

result  of  improper  or  excessive  feeding,  of  faulty  digestion,  or 
of  defective  bowel  evacuation,  substances  are  absorbed  into 
the  circulation  which  act  upon  the  arterial  and  capillary 
walls,  leading  to  an  abnormal  degree  of  contraction  of  the 
vessels.  The  effect  varies  with  the  intensity  of  the  cause  ; 
the  duration  of  the  effect  upon  the  continuance  of  the  cause. 

When  the  major  proposition  is  grasped,  it  unerringly 
follows  that  there  must  be  minor  degrees  of  the  condition 
we  have  pictured. 

The  acceptance  of  this  proposition  leads  to  the  under- 
standing of  the  beginning  of  things — it  shows  the  first  steps 
in  a  process  which  has  only  been  known  in  its  fully 
developed  stage  and  for  the  explanation  of  which  there  has 
been  a  continuously  expressed  desire.  The  arterial  contrac- 
tion caused  by  substances  present  in  the  circulation  is  the 
first  step  in  the  causation  of  arterio-sclerosis ;  and,  if  there 
be  no  kidney  disease,  the  substances  which  cause  the 
contraction  are  absorbed  from  the  alimentary  tract,  and  are 
the  product  in  one  form  or  another  of  what  has  been 
swallowed  in  the  form  of  necessary  aliment  or  of  unnecessary 
indulgence.  It  is  necessary  to  state  the  position  thus,  for 
the  question,  as  will  presently  be  seen,  is  not  confined  to  the 
simple  point  of  excess  in  quantity  or  indulgence  in  what  may 
be  regarded  as  essentially  injurious  in  virtue  of  its  nature. 

Behind  the  questions  of  quantity  and  character  lie  the 
factors  of  inefficiency  or  disorder  of  the  gastro-intestinal 
functions.  These  are  factors  which  it  seems  to  me  have 
been  almost  wholly  overlooked.  That  indigestion  in  its 
various  forms,  particularly  when  associated,  as  it  commonly 
is,  with  definite  constipation,  or  with  incomplete  bowel 
evacuation,  should  be  the  commonest  of  all  causes  of  vessel 
constriction  gives  to  the  disorder  a  significance  which  has 
not  commonly  been  appreciated.  In  the  great  majority  of 
cases  of  the  kind  indicated  it  will  be  found  that  arterial 
hypertonus  is  present.  The  thickening  is  not  necessarily 
great,  and,  when  it  is  associated  with  a  somewhat  small  and 
feeble  pulse  wave,  there  is  such  a  marked  absence  of  what 
is  known  as  tension,  that  the  thickening  is  not  even 
recognised,  and  so  no  deviation  from  the  normal  is  noted, 
beyond  the  smallness   of  the  pulse.      In   other   cases,  if  the 

99 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

thickeuing  of  the  artery  is  recognised  it  is  regarded  as  arterio- 
sclerosis, and  when  it  occurs  in  a  young  or  middle-aged 
person  it  is  looked  upon  as  an  indication  that  so-called 
"  senile  degeneration  "  has  already  begun.  Such  a  conception 
is  undeniably  prevalent,  and  gives  support  to  its  own 
falseness  by  ultimately  leading  to  the  result  suggested.  It 
becomes  thus  a  matter  of  fundamental  importance  to 
recognise  the  hypertonic  thickening  of  arteries ;  and  to 
understand  that  the  hypertouus,  in  such  cases  as  are  here 
indicated,  is  due  to  deleterious  substances  present  in  the  blood 
irritating  or  stimulating  the  vessel  wall ;  and  that  these 
substances  are  absorbed  from  the  intestinal  tract.  The 
nature  of  these  substances  has  been  already  referred  to. 
The  responsiveness  of  the  arteries  to  them  becomes  very 
striking  once  the  correctness  of  the  proposition  is 
tested. 

This,  I  contend,  is  the  first  step  towards  the  production 
of  arterio-sclerosis  in  a  vast  number  of  instances.  Whatever 
alimentary  and  intestinal  conditions  cause  hypertonus  only 
require  to  be  continued  to  produce  sclerosis,  if  cardiac  vigour 
be  at  the  same  time  sustained,  as  it  frequently  is. 

It  is  perhaps  necessary  to  definitely  say  that,  while  stating 
the  foregoing  proposition,  it  is  not  to  be  inferred  that  I  mean 
anything  beyond  what  I  state.  The  spare  feeder  may  develop 
arterio-sclerosis  earlier  than  the  big  feeder,  the  moderate 
drinker  develop  greater  vessel  changes  than  the  man  who 
occasionally  gets  drunk.  If  the  big  feeder  and  moderate 
drinker  has  good  digestion  and  free  bowel  evacuation  daily, 
as  such  people  frequently  have,  he  may  not  devolop  arterio- 
sclerosis till  late  in  life.  Nothing  impedes  advance  so  much 
as  strong  one-sided  statements,  which  usually  enjoy  the  position 
of  maintaining  but  a  fragment  of  truth.  While  arterio-sclerosis 
might  be,  on  a  partial  view  of  the  position,  represented  as 
merely  a  question  of  food  and  drink,  the  contention  would  be 
so  misleading  as  to  make  it  untrue,  for  it  would  leave  out  of 
account  the  spare  feeder  and  the  teetotaler,  who,  if  he  be  a 
dyspeptic  or  the  victim  of  habitual  constipation,  will  assuredly 
supply  in  middle  life  a  typical  example  of  "  premature  arterial 
degeneration."  It  is  the  faculty  of  dealing  efficiently  with 
the  intake,  and  the  easy  and  complete  removal  of  waste  and 

lOO 


FOOD,  DIGESTION,  CONSTIPATION,  AND  ALCOHOL 

excrement,  which  postpone  vessel  changes  in  many  a  man 
who  indulges  his  palate  as  his  abstemious  contemporary  dare 
not  do,  under  the  risk  of  acute  poisoning.  It  is  here  that 
the  explanation  lies  of  the  marked  diversity  of  opinion  held  as 
to  the  influence  of  food  and  of  alcoholic  drinks  in  producing 
vessel  changes.  It  is  a  fact  that  neither  the  big  flesh-eater, 
nor  the  man  wdio  daily  partakes  of  wine,  spirits,  or  beer, 
necessarily  shows  vessel  changes  early  in  life,  and  yet  there 
seems  to  me  to  be  no  doubt  that  in  other  men  these  things 
lead  to  vessel  changes.  In  the  former  class  digestion  is  fault- 
less  and  elimination  perfect ;  in  the  latter,  the  first  may  hold 
and  the  second  fail.  So  it  is  wdth  the  spare  feeder :  he  may 
digest  and  eliminate  efficiently  up  to  his  particular  level  and 
capacity  ;  while  an  equally  spare  feeder  may  be  using  a  dietary 
not  suitable  to  his  standard  of  digestive  capacity  and  excretory 
efficiency  :  of  the  two,  the  former  shows  soft  vessels,  the  latter 
thickened  vessels. 

When  it  is  understood  that  it  is  not  necessarily  the 
character  of  the  materials  which  determine  the  vessel  changes, 
what  has  hitherto  been  a  difficulty  disappears.  We  need  no 
longer  consider  which  is  the  right  and  which  the  wrong  view, 
for,  as  is  usually  found  when  the  experience  of  competent 
observers  is  conflicting,  they  have  each  got  only  a  bit  of  the 
truth.  It  is  not  any  special  poison  in  the  material,  but  the 
presence  of  waste  or  of  absorbed  poison  in  the  blood,  that 
determines  vessel  changes — the  waste  may  be  the  waste  of 
the  physiological  wear  of  tissues ;  it  may  be  the  waste  of  un- 
utilised pabulum,  unused  because  excessive  in  amount.  The 
name  of  the  special  purin  body  in  the  special  food  of  the 
particular  individual  may  be  safely  left  to  the  pure  chemical 
pathologist.  For  clinical  and  practical  purposes  the  essential 
fact  is  that  the  tightening  up  of  the  arteries  is  due  to  tlie 
presence  of  substances  in  the  blood  which  ought  not  to  be 
there  in  any  sufficient  amount  to  keep  up  vessel  con- 
striction. 

I  even  carry  my  contentions  further  than  this.  To  me 
the  influence  of  the  condition  of  the  blood  upon  the  tone  of 
the  arteries  is  so  certain  that  I  have  realised  for  some  time 
that  in  many  cases  the  recognition  of  arterial  hypertonus 
suggests  either  disordered  metaliolism  or  constipation,  and  I 

lOI 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

am  struck  with  the  number  of  instances  in  which  the  surmise 
proves  to  be  correct  and  becomes  the  basis  of  successful 
treatment. 

There  is  tlius  produced  a  chain  of  graduated  links,  each 
link  an  example  of  the  same  underlying  physiological  proposi- 
tion, which  must,  I  think,  rank  as  a  law — namely,  that  vessel 
tone  is  influenced  and  determined  by  blood  composition,  and 
that  to  us  as  practitioners  of  healing  the  important  point  is 
that  blood  composition  is  determined,  directly  or  indirectly,  by 
absorption  from  the  intestinal  tract. 

It  will  not  be  altogether  unprofitable  to  devote  some 
further  words  to  the  consideration  of  blood  composition. 
When  we  do  so  we  are  forced  to  recognise  that  it  must  show 
much  more  subtle  variations,  as  regards  the  extraneous  sub- 
stances which  may  be  present  in  it,  than  the  ordinary  chemical 
composition  as  supplied  by  physiology  suggests.  The  blood- 
content  is  in  the  first  place  influenced  by  the  food  taken. 
The  processes  in  digestion  cannot  be  regarded  as  picking 
out  and  selecting  merely  what  is  suitable  from  what  is 
swallowed :  all  substances  are  acted  upon  so  that  their  soluble 
constituents  can  be  absorbed,  either  into  the  lymph  system  or 
directly  into  the  blood  system.  In  the  latter  case,  the  liver 
serves  not  only  as  a  living  filter-bed  but  as  a  chemical 
"  clearing-house "  for  the  blood  brought  by  the  portal  vein 
from  the  alimentary  tract,  before  it  passes  on  into  the 
systemic  system.  When,  on  the  other  hand,  substances 
pass  directly  into  the  lymph  system,  only  the  lymph  glands 
interpose  between  them  and  the  systemic  blood  system ; 
and  it  is  not  known  that  these  glands  have  any  chemical  duty 
to  perform  in  this  connection,  although  they  filter  out  solid 
particles  whether  these  be  living  or  dead.  In  either  case 
there  is  of  course  no  doubt  that  substances  reach  the  blood, 
by  one  or  other  channel,  which  are  not  necessary  for  the 
physiological  requirements  of  the  body.  That  this  occurs  is 
of  course  fully  established  by  our  everyday  clinical  observa- 
tions and  therapeutic  procedures.  The  fact  that  certain  foods 
in  some  persons  produce  urticaria  is  abundant  proof  of  this, 
even  were  there  no  other.  The  influence  of  alcohol,  the 
effects  produced  by  the  drugs  we  use,  are  all  brought  about 
by  the  passage  into  the  blood  of  the  unmodified  substances 

1 02 


FOOD,  DIGESTION,  CONSTIPATION,  AND  ALCOHOL 

themselves,  or  as  they  are  modified  in  their  passage  through 
the  ahmentary  system;  for  it  is  to  be  realised  that  both 
processes  occur. 

Although  this  is  so  evident  that  I  do  not  suppose  it  will 
be  questioned  in  any  quarter,  I  am  not  aware  that  physio- 
logical chemistry  is  in  a  position  to  determine  what  the  subtle 
substances  are  in  the  blood  which  produce  urticaria  after 
the  ingestion  of  certain  things.  Yet  it  would  be  the  veriest 
folly  for  the  clinician  to  doubt  the  existence  of  such  sub- 
stances ;  and  the  clinician's  observations  ought  to  stimulate 
physiological  and  chemical  research. 

I  say  so  much  because  I  am  not  competent  to  discuss 
with  any  semblance  of  authority  the   subtle   changes  which 
must  be  acknowledged  as  occurring  in  the  blood  as  the  result 
of  the  various  foods  and  fluids  partaken  of,  or  of   the  manner 
in  which  they  are  dealt  with  in  the  alimentary  tract  from  the 
stomach  onwards,  including  the  final   ejection   of  their  refuse 
and  waste.      At  the  same  time,  I  fully  recognise  the  value  of 
the  investigations  which  have  been  made  of  the  purin  group 
of  bodies  by  Dr.  Walker  Hall  and  others ;  and  of  the  suggest- 
iveness  of  the  proposition  that  these  bodies  are  contained  in 
common    articles    of    diet,    pass   from    the   alimentary   tract 
practically    unchanged    into    the    circulation,     and     exercise 
certain     undesirable     influences.      This    is    the    direction    in 
which  research  will  no  doubt  be  continued  until  knowledge 
becomes  fuller  and  more  assured ;  meanwhile,  that  work  may 
already  be  accepted  as  confirmation  of   the  major  proposition 
that  substances  are  taken  up  from  the  alimentary  tract  into 
the  blood  which  directly  influence  the  arterial  and  capillary 
walls.      I  have  already  dealt  with  the  evidence  from  experi- 
mental investigation  proving  the  direct   effect  of  substances 
in  the  blood,  or  circulating  fluid,  upon  the  vessel  wall,  leading 
to    increased    tone    or    contraction ;    and    that   the   common 
conception    of    the  vessels  merely   responding  to   vasomotor 
nerve  impulses  has  to  be  abandoned,  and  the  wider  proposition 
adopted.      Having  thus  far  carried  my  contentions,  it  remains 
to  be  shown  what  clinical  evidence  is  availal^le,  not  only  in 
support  of  these  contentions,  but  as  indicating  more  definitely 
the  dietetic  substances   which  act   most   potently ;    whether 
they    act    in    virtue    of     their    essential    composition,    their 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

excessive  quantity,  or  as  a  result  of  secondary  changes  taking 
place  in  them  in  the  alimentary  tract. 

In  the  first  place  stands  the  question  as  to  whether  the 
kind  of  food  is  of  any  practical  importance  ?  There  is  no 
doubt  that  the  great  bulk  of  clinical  opinion  and  experience, 
both  in  the  past  and  the  present,  points  to  the  more  highly 
proteid  foods  producing  effects  not  produced  by  the  carbo- 
hydrate foods.  Free  and  abundant  flesh-eating  has  come  to 
be  regarded  as  leading  to  "  heightening  of  blood-pressure " 
and  to  consequent  arterial  changes.  This  appears  to  be  the 
view  expressed  in  recent  writings  on  subjects  where  blood- 
pressure  and  "  arterial  tension  "  are  included  in  the  considera- 
tion of  the  questions  which  are  discussed.  It  is  so  prevalent 
that  it  would  be  invidious  to  single  out  individual  examples 
when  our  aim  is  to  deal  with  the  whole  question  of  blood- 
pressure  and  vessel-changes  from  the  constructive  side,  and  to 
avoid  the  polemical  tone  which  destructive  criticism  can 
hardly  avoid.  With  the  common  view  as  to  the  injurious 
effects  of  a  large  proteid  dietary  I  wholly  agree.  At  the 
same  time,  the  common  view  requires  important  modifications 
to  give  it  its  full  clinical  value.  The  mental  picture  is  too 
much  confined  to  the  man  who  eats  largely  and  becomes 
florid  and  "  plethoric "  as  a  result — the  man  of  Herculean 
digestion.  For  clinical  purposes,  it  is  essential  to  recognise 
the  large  class  of  persons  who  eat  moderately,  or  are  even 
regarded  as  small  eaters,  but  whose  digestive  functions  or 
alimentary-tract  processes  are  faulty.  In  these  persons  even 
their  spare  proteid  dietary  is  excessive.  In  some  cases  the 
error  appears  to  be  digestive,  but  more  commonly  the  essential 
error  is  constipation.  Even  when  there  is  digestive  disorder, 
it  may  be  the  result  of  constipation  as  well  as  the  cause  of  it. 
Proteid  food  retained  in  the  intestine  putrefies  and  raises  the 
virulence  of  the  colon  group  of  bacilli,  and  the  products  are 
absorbed,  as  has  been  already  indicated.  In  fact,  the  factor  of 
putrefaction  seems  to  me  to  be  so  common,  as  a  result  of  the 
prevailing  constipation,  that  I  give  it  a  foremost  place.  I  do 
not  find  indications  of  proteid  food  being  injurious  in  moderate 
feeders  who  have  very  free  daily  bowel  evacuation.  The  cult 
that  holds  that  no  man  eats  flesh  with  impunity  is  as 
unscientific  as   extremes   usually   are.      If    the   spare  feeder, 

104 


FOOD,  DIGESTION,  CONSTIPATION,  AND  ALCOHOL 

in  spite  of  his  abstemiousness,  suffers  auto  -  intoxication 
from  putrefying  proteid,  he  will  find  material  comfort  in  a 
dietary  which  does  not  so  putrefy ;  but  the  primary  fault  is 
in  the  alimentary  tract,  not  in  the  food  itself.  Putting  aside 
the  question  of  mere  vulgar  excess,  what  one  finds  in  the 
class  of  case  I  have  been  dealing  with  is,  that  there  are  usuallv 
subjective  symptoms  of  various  kinds  commonly  attributed  to 
"  biliousness  "  or  to  "  liver,"  that  along  with  these  the  radial 
artery  is  hypertonic,  and  the  urine  indicates  the  presence 
of  intestinal  putrefaction.  In  such  cases  there  is  no  doubt 
there  are  deleterious  substances  present  in  the  bbjod,  for  they 
are  excreted  in  the  urine ;  and  it  seems  to  me  certain  that 
they  act  directly  upon  the  arterial  wall,  leading  to  a  hyper- 
tonic contraction  of  it.  Certain  it  is  that  if  the  Ijowel  be 
unloaded  the  hypertonus  relaxes.  A  dose  of  mercury  may 
have  the  same  effect,  even  before  it  acts  as  a  laxative, 
presumably  owing  to  some  influence  it  has  directly  or 
indirectly  on  the  intestinal  contents. 

There  is  some  difficulty  in  turning  people's  minds  round 
to  look  not  so  much  at  absolute  quantity  as  at  the  use  made 
of  what  is  taken.  The  importance  of  intestinal  putrefaction 
has  not  been  known ;  and  it  has  not  been  widely  realised  that 
carbohydrate  foods  ferment  but  do  not  putrefy. 

I  have  hitherto  in  ^'ain  sought  for  evidence  that  carbo- 
hydrate food  leads  to  the  arterial  hypertonus  which  I  have 
referred  to  as  resulting  from  the  putrefaction  of  proteid. 

The  position  may  be  summarised  thus :  an  excessive 
flesh  dietary,  even  when  digested,  is  hurtful  because  of  the 
excess  of  material  absorbed,  which  cannot  be  utilised  and  has 
to  be  eliminated.  When  putrefaction  occurs,  whether  it  be 
in  well-digested  or  ill-digested  flesh  foods,  the  products  are 
highly  injurious.  The  injurious  effect  is  shown  in  the  arteries 
by  hypertonic  contraction  and  so-called  "  high  tension,"  and 
this  ultimately  leads  to  arterio-sclerosis.  Carljohydrates  do 
not  have  the  same  kind  of  effect. 

The  symptoms  which  are  popularly  and  vaguely  defined 
as  gouty  or  suppressed  gout  are  all  referable  to  the  defects 
which  have  been  indicated.  They  are  all  due  to  the  presence 
of  waste  retained,  or  deleterious  substances  absorbed  and  not 
readily    excreted.       The     mental     depression,     the     physical 

105 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

weariness,  the  bilious  attack,  all  have  their  source  here,  and 
they  will  be  found  to  be  always  accompanied  by  hypertonic 
arterial  contraction.  As  we  relax  the  vessels  by  treatment 
the  symptoms  disappear,  and,  if  we  can  so  order  life  as  to 
prevent  hypertonic  contraction,  there  is  an  absence  of  the 
gouty  symptoms. 

Believing  the  position  to  be  such  as  is  here  indicated,  it 
follows  that  I  place  the  condition  of  the  alimentary  tract  in 
the  forefront  of  the  causes  which  lead  to  arterio-sclerosis,  with 
all  its  manifestations,  and  all  its  disastrous  consequences,  in- 
cluding the  shortening  of  life. 

I  cannot  pass  from  the  alimentary  tract  without  referring 
specifically  to  the  effect  of  beer  and  spirit  drinking  upon  the 
vessels.  Acute  alcoholism  is  dealt  with  in  a  separate 
chapter,  but  from  what  I  have  seen  there  seems  to  me  to  be 
no  doubt  that  in  some  persons  the  steady  daily  use  of  beer 
or  whisky  leads  to  pronounced  arterio-sclerosis.  I  append  a 
short  note  of  a  few  cases  illustrating  this  point.  It  is  not 
the  invariable  result  in  all  persons,  as  will  be  seen  from  the 
subsequent  chapter  dealing  with  alcoholism.  The  fact  is  that 
the  effects  of  alcohol  afford  but  another  illustration  of  what  I 
have  already  tried  to  enforce,  that  it  is  altogether  wrong  to 
take  up  the  position  that  the  same  substance  produces  the 
same  XDhysiological  or  pathological  results  in  all  persons. 
An  excessive  proteid  dietary  is  entitled  to  rank  alongside 
alcohol ;  but  it  is  probable  that  constipation  is  the  cause 
of  as  much  arterial  change  in  the  people  of  Britain  as  either 
the  one  or  the  other. 


THE   EFFECT    OF    THE   ALIMENTARY   SYSTEM    ON 
SCLEROSED   VESSELS 

From  what  has  been  said  with  regard  to  the  influence  of 
the  alimentary  system  in  leading  to  hypertonus  and  ultimately 
to  sclerosis,  and  bearing  in  mind  the  contention  that  sclerosed 
vessels  readily  become  hypertonic,  the  further  statement  will 
be  anticipated,  namely,  that  when  sclerosis  is  established,  the 
same  circumstances  or  conditions  in  the  alimentary  tract  con- 
tinue to  act.  The  point  is,  however,  of  such  great  practical 
importance  that  it  is  desirable  to  accentuate  it  by  specially 

1 06 


ALIMENTARY  SYSTEM  AND  THE  ADRENALS 

referring  to  it  here.  In  elderly  people  with  sclerosed  vessels 
the  influence  of  this  tract  is  very  striking,  when  the  recog- 
nition of  hypertonus  becomes  a  matter  of  routine  observation. 
The  effect  of  proteid  food  in  them  is  in  my  experience  quite 
beyond  question.  Whether,  however,  it  be  the  supply  of 
proteid  in  excess  of  the  needs  of  the  inactive  body,  or 
intestinal  putrefaction  and  constipation  which  supplies  the 
precise  irritant,  is  not  easy  to  determine ;  but  in  many  cases 
the  two  factors  are  conjoined. 

The  sclerosed  vessels  are  indeed  remarkably  sensitive  to 
the  irritant  or  stimulant,  whatever  it  be.  I  do  not  attempt 
to  offer  any  explanation,  but  I  am  convinced  that  it  is  a 
clinical  fact.  The  sensitiveness  may  become  marked  even  to 
impressions  conveyed  through  the  vasomotor  centre,  as  I 
have  shown  in  Chapter  XV.,  when  dealing  with  angina  pectoris. 
The  practical  and  clinical  bearing  of  the  fact  is  that  the 
irritability  of  the  vessels  can  be  in  a  great  measure  controlled 
by  an  austere  dietary,  conducted  on  the  lines  indicated  by 
recent  and  more  accurate  physiological  investigations. 

In  elderly  or  old  people  it  will  be  found  that  there  is  no 
surer  guide  to  the  right  line  to  be  taken  in  their  management 
and  treatment  than  by  the  recognition  of  whether  hypertonus 
is  or  is  not  present. 

In  subsequent  chapters  cases  are  given  in  which  the 
influence  of  food  or  of  constipation  is  shown ;  and  on  the 
other  hand,  the  effect  of  bowel  evacuation  is  seen.  It  seems, 
therefore,  unnecessary  to  elaborate  this  matter  more  fully  here, 
but  I  hope  I  have  said  enougli  to  carry  the  conviction  of  the 
importance  of  this  side  of  our  subject.  As  having  some 
bearing  upon  the  following  section,  I  may  say  that  I  have 
tried  thyroid  in  these  cases,  and  it  seemed  so  definitely  un- 
satisfactory that  I  have  ceased  its  use. 

THE  INFLUENCE  OF  THE  ALIMENTARY  SYSTEM  ON 
THE  ADRENALS 

In  an  address  delivered  to  the  Derby  Medical  Society,  and 
published  in  the  British  McAlical  Journal  on  4th  June  1904, 
I  suggested  that  the  effect  of  a  rich  proteid  diet  in  causing 
hypertonic  contraction  of   vessels  might   act  by  stimulating 

107 


INFLUENCE  OF   THE  ALIMENTARY  SYSTEM 

the  secretion  of  the  suprarenal  glands,  extracts  of  their 
medullary  portion  being  known  to  have  this  constrictor  action 
on  the  vessels.  Three  years  of  added  experience  have  drawn 
me  further  away  from  this  idea  :  while  the  effect  of  absorption 
directly  into  the  blood  from  the  intestinal  tract  seems  a  more 
satisfactory  explanation  of  such  a  clinical  phenomenon  as  the 
removal  of  hypertonus  by  laxatives.  As  these  pages,  how- 
ever, were  being  corrected  for  the  press,  the  very  able  and 
suggestive  address  delivered  by  Dr.  H.  D.  EoUeston  to  the 
Canadian  Medical  Association  appeared  in  The  Lancet.  In 
that  address  he  referred  to  the  suggestion  mentioned  above. 
It  is  not,  however,  for  that  reason  I  refer  to  it  now,  but 
because  his  address,  while  presenting  a  vivid  picture  of 
experimental  and  clinical  observations  on  the  problems  which 
surround  the  suprarenals,  brought  back  an  idea  which  suggested 
itself  to  me  years  ago,  when,  as  pathologist  to  the  Eoyal 
Infirmary,  I  was  methodically  examining  these  glands.  The 
idea  was  that  the  cortical  part  of  the  gland  was  for  the 
destruction  or  transformation  of  the  substances  present  in  the 
medullary  portion.  This  idea  would  explain  the  apparently 
curious  fact  that  extracts  of  the  latter  have  such  a  marked 
physiological  action,  while,  so  far  as  is  known,  the  cortex  has 
no  such  action.  Following  this  idea  further,  it  may  be  that 
the  active  principle  in  the  medulla  may  be  taken  from  the 
blood  as  a  harmful  substance,  and  altered  in  its  passage 
through  the  cells  of  the  cortex  into  a  harmless  substance. 
Were  this  found  to  be  the  true  view,  it  would  easily  follow 
that  an  excess  of  proteid  absorption  or  of  other  substances 
from  the  intestine  throws  a  greater  strain  on  the  glands  than 
they  were  equal  to,  and  that  constrictor  substances  accumu- 
late by  retention  in  the  blood.  As  giving  some  little 
support  to  this  suggestion,  I  may  add  my  impression  that  in 
advanced  life  the  cortical  part  of  these  glands  is  relatively 
small.  If  these  speculations  turned  out  to  be  correct,  they 
would  explain  the  sensitiveness  of  sclerosed  vessels  in  elderly 
persons  referred  to  in  the  previous  section.  In  this  particular 
region  of  speculation  no  harm  follows  a  wrong  view,  and, 
when  Dr.  Eolleston  regards  his  imaginings  as  "  somewhat 
wild  speculation,"  I  would  remark,  that  such  speculations  may 
become  the  facts  of  a  later  date.      It  would  only  mean  that 

loS 


ILLUSTRATIVE  CASES 

the   glands   were    excreting   and  not   producing   the    pressor 
substance  found  in  their  medullarj  part. 

CASES   ILLUSTEATING   THE    FOEEGOING   CONTENTIONS 

Excessive  'proteid  dietary  loith  thick  and  tortuous  radials — 
recurring  aphasia 

Case  10. — E.  S.  K.,  a  man  in  middle  life,  sent  by  Dr. 
M'Ewan  of  Prestonpans,  with  a  history  of  temporary  attacks 
of  partial  and  complete  aphasia.  The  radial  arteries  were  very 
thick  and  tortuous.  The  heart  extended  to  an  inch  beyond 
the  nipple  line.  The  urine  contained  no  albumin,  the  specific 
gravity  was  1011.  He  usually  had  to  get  up  in  the  night  to 
pass  water.  On  inquiry,  he  acknowledged  that  he  had  "  lived 
on  beef  " ;  he  took  beefsteak  to  breakfast,  broth  and  beef  to 
dinner,  and  beef  to  supper.  There  was  no  other  factor  in  his 
history  to  explain  the  arterial  thickening. 

Excessive  'pToteicl  dietary  vjith  thick  radial  arteries 
in  a  young  man 

Case  11. — T.  N.,  set.  25,  butcher,  Fife,  seen  at  the  Eoyal 
Infirmary,  15th  November  1905.  He  complained  of  pain 
in  the  stomach  in  the  forenoon,  and  sometimes  in  the  evening. 
The  pain  at  first  was  in  the  pit  of  the  stomach,  but  more 
recently  it  was  "  working  to  the  left."  The  bowels  moved 
daily.  The  doctor  he  had  consulted  thought  the  pain  was 
due  to  a  strain.  The  radial  arteries  were  markedly  thickened. 
The  heart  was  normal,  and  there  was  no  albumin  in  the  urine. 
The  thickening  of  his  vessels  was  so  marked,  and  as  there 
was  no  evidence  or  history  of  syphilis,  I  made  special 
inquiries  as  to  his  diet,  and  found  it  to  be  as  follows :  at 
7  a.m.  he  had  bread  and  butter  and  tea ;  "  breakfast "  was  at 
1 2  noon,  and  consisted  of  half  a  pound  of  steak  and  an  egg ; 
"dinner,"  at  2.30  p.m.,  consisted  of  soup,  another  half-pound 
of  meat,  potatoes,  a  glass  of  milk,  and  rice ;  "  supper,"  7  to  8 
p.m.,  consisted  of  fish,  bread,  and  tea. — I  impressed  upon  him 
the  fact  that  he  was  doing  himself  injury  by  the  amount  of 
flesh  he  was  taking.  I  advised  him  to  take  meat  once  a  day 
only,  and  prescribed  5  grains  of  potassium  iodide  thrice  daily. 

109 


INFLUExNCE  OF  THE  ALIMENTARY  SYSTEM 

Constipation  until  auto-intoxication  and  hypertonic  arteries 

Case  12. — Wm.  A.,  ^et.  41,  an  iron  moulder,  sent  to  the 
Koyal  Infirmary  from  Falkirk,  complained  of  weariness  and 
want  of  strength,  and  as  having  had  a  cold  with  a  little  cough 
for  some  months.  He  brought  a  specimen  of  his  sputum, 
but  it  was  quite  colourless,  and  we  did  not  consider  it 
necessary  to  stain  it  for  tubercle  bacilli.  Examination  of 
his  lungs  and  heart  showed  them  to  be  apparently  healthy. 
The  tongue  was  clean,  with  moist  edge  and  dryish  centre. 
He  had  indefinite  sensations  in  the  abdomen  at  times,  but 
he  had  evidently  paid  no  special  attention  to  them,  and  could 
neither  locate  them  nor  describe  them.  He  had  much 
flatulence.  The  stomach  was  dilated,  reaching  as  low  as  the 
umbilicus,  and  although  it  was  four  hours  since  he  break- 
fasted, his  stomach  was  full  and  splashing.  The  urine 
contained  no  albumin  or  sugar.  The  bowels  moved  nearly 
daily,  but  he  had  to  regulate  them  by  taking  laxatives.  The 
radial  arteries  were  thickened  and  definitely  hypertonic. 
— My  opinion  of  this  case  was  that  the  patient  had  atonic 
dyspepsia  with  gastric  dilatation ;  a  measure  of  constipation ; 
that  the  languor  and  sense  of  weakness  were  the  result  of 
auto-intoxication,  and  that  the  hypertonic  condition  of  the 
arteries  was  to  be  similarly  explained. 

Hypertonus  from  constipation 

Case  13. — Mr.  T.,  ret.  30,  was  being  examined  for  insur- 
ance. He  did  not  smoke ;  there  was  no  sugar  or  albumin  in 
the  urine ;  the  heart  was  normal.  He  had  quite  definite 
hypertonus  of  the  radial  artery,  and  this  was  associated  with 
a  distinctly  costive  habit. 

Constipation  with  precordial  jyain  and  hypertonic  radicds 

Case  14. — N.  P.,  iron  moulder,  set.  20.  This  youth  was 
admitted  to  hospital  suffering  from  recurring  pain  and 
discomfort  in  the  precordia  along  with  symptoms  of  gastric 
disorder.  He  was  constipated,  and  there  was  marked 
hypertonic  thickening  of  his  radials.  The  bowels  were 
regulated  by  a  daily  dose  of  cascara  and   glycerine,  and    a 

I  lO 


ILLUSTRATIVE  CASES 

rhubarb  and  soda  mixture  were  given  for  the  stomach 
condition.  The  pain  disappeared,  and  the  thickening  of  his 
arteries  almost  entirely. 

Cases  illustrating  the  effect  of  Ijecr-drinldnrj  on  the  vessels 

Case  15. — Henry  F.,  aged  36,  engineer,  seen  at  the  Eoyal 
Infirmary  on  5th  September  1906.  He  was  a  repairer  of 
bookbinding  machines,  and  tl^ierefore  travelled  a  good  deal. 
He  complained  of  pain  in  the  back  when  he  stooped,  and 
lately  of  great  giddiness,  especially  when  stooping.  The 
giddiness  had  been  so  severe  that  he  volunteered  the  state- 
ment  that  he  had  nearly  fallen  down  the  hoist  track.  He 
was  a  vigorous,  intelligent-looking  man,  with  a  sallow  com- 
plexion, and  icteric-tinged  conjunctiva.  He  was  married,  and 
had  six  healthy  children.  The  bowels  moved  daily,  but  he 
"  suffers  terribly "  from  flatulence  passing  by  the  bowel. 
The  tongue  was  thickly  coated  in  its  posterior  two-thirds. 
There  was  nothing  to  note  in  the  thorax  or  abdomen.  The 
urine  contained  neither  albumin  nor  sugar :  he  said  it  varied 
in  colour :  the  sample  we  saw  was  rather  pale  in  colour. 
The  radial  arteries  were  markedly  thickened  and  hard. 
He  was  an  Englishman,  and  every  night  nearly  drank  two 
or  three  glasses  of  beer.  He  never  exceeded.  He  had  no 
appetite  for  breakfast. — I  prescribed  for  him  a  mixture 
containing  sahcylate  of  sodium  and  iodide  of  potassium  to  be 
taken  thrice  daily ;  a  laxative  pill  to  be  taken  nightly ;  and 
strongly  advised  him  to  stop  his  beer. 

Case  16.- — Thos.  X.,  aged  37,  seen  at  the  Eoyal  Infirmary 
on  5th  September  1906,  brewery  carter,  delivering  casks  of 
beer  to  the  public-houses  in  the  city.  Complained  of  heavi- 
ness in  his  belly  and  of  being  "  awful  giddy  whiles."  He 
is  a  big,  stout,  heavy  man.  There  was  a  little  tremulousness 
about  the  mouth  when  he  was  being  questioned  about  his  beer- 
drinking.  There  was  nothing  to  be  made  out  in  the  abdomen. 
The  bowels  moved  daily.  He  was  not  sure  as  to  the  amount 
of  beer  he  drank  daily,  but  it  seemed  certain  that  his  habit 
was  to  drink  whenever  he  had  the  opportunity,  either  at  the 
brewery  or  when  offered  it  at  the  j)ublic-houses  at  which  he 

I II 


INFLUENCE  OF  THE  ALIMENTARY  SYSTEM 

delivered.  He  had  been  over  twenty  years  working  about 
breweries.  The  urine  contained  no  albumin.  The  radial 
arteries  were  so  thick  and  hard  that  they  might  almost  have 
been  called  rigid^ — they  were  comparatively  small  vessels,  as  if 
they  were  diminished  in  size  from  hypertonic  contraction. — 
I  ordered  him  a  laxative  pill  to  be  taken  nightly  for  a  week ; 
20  minims  of  sp.  etheris  nitrosi  to  be  taken  thrice  daily,  to 
give  up  beer  absolutely,  and  to  report  himself  to  me  in  a  few  days. 
10th  Septcmhcr. — Eeported  himself  at  the  ward.  Feel- 
ing much  Ijetter.  Giddiness  gone.  Eadial  much  larger  and 
more  compressible — now  a  thick  vessel  not  suggesting  rigidity  : 
Oliver  pressure,  170  ;  Gartner,  150. 

Extreme  arteriosclerosis  from  the  daily  use  of  alcohol  for 
many  years 

Case.  17. — Wm  S.,  ret.  64,  came  to  the  Infirmary  complain- 
ing of  pain  in  the  back  of  his  head,  in  the  temples,  and  over 
the  vertex,  also  of  giddiness.  He  was  a  healthy-looking,  well- 
nourished  man  with  a  slightly  florid  complexion,  but  older- 
looking  than  his  years.  Both  temporal  arteries  were 
prominent  and  were  the  thickest  and  hardest  temporals  I  had 
ever  seen — in  size  and  hardness  they  almost  felt  like  pen- 
holders. The  radial  arteries  were  in  a  similar  condition,  al- 
though not  quite  so  extreme.  There  was  no  albumin  in  the 
urine.  He  assured  me  he  had  always  been  a  steady  man,  had 
never  drunk  to  excess  or  to  do  himself  "any  harm."  There 
was  no  history  of  syphilis,  of  rheumatism,  or  of  gout.  He 
never  suffered  from  dyspepsia,  and  his  bowels  always  moved 
daily  and  freely.  In  fact,  there  seemed  to  be  no  explanation 
obtainable  of  the  extreme  sclerosis.  With  more  detailed 
questioning  it  came  out  that  up  until  within  the  last  few 
years  he  had  spent  his  working  years  since  a  lad  as  an 
assistant  to  licensed  grocers  and  wine  merchants,  and  that 
during  all  those  years  he  had  daily  taken  spirits. 

REFERENCES. 

Chittenden,  Physiological  Economy  in  Nutrition,  1905.  Herter, 
Chemical  Pathology,  1902.  Broadbent,  loc.  cit.  p.  155;  Leonard 
Hill,  loc.  cit.  Walker  Hall,  The  Purin  Bodies,  1903.  W.  Russell, 
Caledonian  Med.  Journ.,  April  or  July  1905.  H.  D.  Rolleston,  The 
Lancet,  Sept.  28,  1907. 

112 


CHAPTER   XIII 

H.EMOMANOMETER  PRESSURES    IN  CASES  OF 
ACUTE  ALCOHOLISM 

THE    VALUE    OF   A   VASO-DILATOR   ADDED    TO    THE 
ORDINARY   TREATMENT. 

In  this  chapter  I  propose  to  record  observations  made  by 
myself  and  my  chnical  assistant,  Dr.  Green,  on  patients  in 
Ward  3  of  the  Edinburgh  Eoyal  Infirmary,  and  to  consider 
these  observations  as  iUustrating  and  supporting  my  main 
contentions  regarding  the  records  of  so-caUed  blood-pressure. 
At  the  same  time  it  will  be  shown  that  here  also  the  records 
are  of  much  interest,  and,  when  rightly  understood,  of  decided 
clinical  value. 

The  cases  to  be  dealt  with  were  cases  of  acute  alcoholism, 
differing  in  intensity,  but  all  sufficiently  pronounced  to  have 
been  admitted  to  the  ward  provided  for  the  reception  of 
patients  suffering  from  "  incidental  delirium."  The  patients 
whose  conditions  are  dealt  with  were  all  in  the  midst  of  a 
bout  of  heavy  drinking,  either  the  victims  of  hallucinations 
of  sight  or  hearing,  or  in  the  stage  of  yattering  incoherence 
with  tremor  and  restlessness.  In  the  stage  of  tremor  and 
constant  muscular  movement  it  was  of  course  impossible 
to  make  accurate  hjemomanometer  observations ;  but  this 
phase  might  not  develop  until  the  patient  had  been  in 
hospital  for  twenty-four  hours  or  longer :  in  one  case  it  did 
not  develop  until  he  had  been  in  the  ward  for  three  days  ;  and, 
having  been  in  on  several  previous  occasions,  it  was  known 
that  this  was  the  usual  time  for  his  delirium  to  begin.  In 
this  way  hgemomanometer  readings  were  sometimes  obtained 
before  delirium  developed. 

The  first  generalisation  I  have  made  from  these  cases  is 
H  113 


H^MOMANOMETER  PRESSURES 

that  not  in  all  cases  is  the  arterial  pressure  high ;  the  second 
is  that  in  the  great  majority  of  cases  the  pressure  is  relatively 
high  to  begin  with,  and  falls  as  the  patient  improves.  In 
the  latter  group  the  pressure  was  usually  about  150  and  fell 
to  115  to  125  or  thereby,  if  the  arteries  were  not  sclerosed. 
When  they  were  sclerosed  the  readings  to  begin  with  were 
much  higher  than  this,  and  did  not  fall  as  low  as  1 5  0  although 
the  patient  had  recovered. 

GROUP  I. — CASES  WITH  LOW  PRESSURES. 

As  examples  of  what  may  be  regarded  as  low  pressure  in 
acute  alcoholism,  the  following  cases  may  be  given : — 

Case  18. — A.  A.,  male,  aged  36,  was  seen  by  one  of  the 
resident  physicians,  and  admitted  to  Ward  3  on  8th  January 
1907.  On  admission  the  patient  was  excited,  with  a  rapid 
pulse,  a  moist  skin,  and  was  stated  to  have  spoken  of  seeing 
various  animals  crawling  on  the  walls.  He  was  given  30 
grains  of  bromide  of  potassium  and  20  grains  of  chloral 
hydrate.  He  was  admitted  at  9.45  p.m.,  but  he  was  not 
asleep  until  4  a.m.  When  I  saw  him  on  the  9  th  his 
IDressure  at  12.30  p.m.  was  only  115,  the  radial  artery  was 
soft,  and  the  pulse  of  fair  strength.  He  was  still  very 
tremulous.  He  was  ordered  a  mixture  containing  strychnine, 
digitalis,  and  valerian.  On  the  13th  his  pressure  was  95  ; 
he  was  feeling  very  well.  He  was  allowed  to  go  home  on 
the  14th. 

Case  1 9.^ — W.M.,  aged  3  3,  maltman,  was  admitted  to  Ward 
3  on  14th  January  1907.  He  drank  beer  and  whisky.  On 
admission  he  was  restless  and  tremulous,  and  was  given  20 
grains  of  chloral.  On  the  15th  when  I  saw  him  his  pressure 
was  120.  He  was  a  plump  man  with  a  plump,  fat  arm.  On 
the  17th  the  pressure  had  fallen  to  110,  the  vessel  wall  being 
soft  with  no  thickening. 

The  following  four  cases  of  acute  alcoholism  further 
illustrate  the  state  of  the  arterial  wall  on  admission,  the  treat- 
ment  given,   and   the   change   in    pressure    after    treatment. 

114 


ACUTE  ALCOHOLISM 

In  all  it  will  be  noted  that  the  pressure,  although  not  high  on 
admission,  fell  still  lower  on  recovery.  In  all  four  cases  the 
relaxation  and  softening  of  the  arterial  wall  was  appreciable  to 
the  finger  as  the  pressure  fell. 


Sex  and 
age. 

Condition  of 
radial  artery. 

Treatment. 

Date. 

Pressure. 

Male  30 

Tightened  up 

Stomach  lavage 

f  March  15 
\       „      16 

120  mm.  Hg. 

105 

Do.    44 
Do.    38 

Do. 
Do. 

Erythrol  and 
chloral 

Erythrol   and 
trional 

f    Jan.     23 
\       ,,       29 
/'      „       18 
I      „       22 

135 
105 

115  (taken  after 
95      treatment 

Do.    50 

Do. 

Iodide,  squill, 
and  digitalis 

(  Slarch    8 
-         „       14 
[       „       15 

hegun) 
115 
105 
100 

GROUP  II. — CASES  IN  WHICH  PRESSURE  WAS  RE- 
LATIVELY HIGH.  THE  EFFECT  OF  A  VASO- 
DILATOR  ADDED    TO   A   HYPNOTIC. 

The  following  cases  belong  to  the  more  common  type,  in 
which  the  pressure  was  relatively  high  on  admission  and  fell 
to  normal  or  to  some  10  degrees  or  so  short  of  normal. 
Some  of  the  cases  illustrate  the  effect  of  a  combination  of 
erythrol  tetranitrate  with  hypnotics — a  comljination  which 
was  suggested  by  my  clinical  assistant,  who  argued  that  the 
sedatives  we  were  using  might  act  more  promptly  if  the 
vessels  were  at  the  same  time  more  promptly  dilated  by 
means  of  erythrol  tetranitrate.  This  combination  has  given 
us  in  some  instances  strikingly  satisfactory  results.  We  have 
so  far  only  followed  this  method  where  the  heemomanometer 
readings  have  been  high,  but  propose  testing  the  effect  of  the 
combination  on  a  more  extensive  scale. 


Case  20. — E.  C,  male,  aged  -46,  was  admitted  to  Ward  3 
by  a  house  physician  on  7th  Jainiary  1907  at  11.30  p.m., 
suffering  from  delirium  tremens — very  tremulous,  and  seeing 
and  picking  up  imaginary  coins  from  the  coverlet  of  his  bed. 
At  1  a.m.  on  the  8th  he  was  given  20  grains  of  chloral,  a  like 

115 


H.EMOMANOMETER  PRESSURES 

close  being  given  at  5  a.m.  He  did  not  sleep  but  was  quiet 
and  muttering  low.  When  I  saw  him  about  noon  he  was 
tremulous,  in  muttering  delirium,  and  his  arteries  were 
like  whipcord.  At  1  i^m.  he  was  given  20  grains  of  trional,' 
half  a  grain  of  erythrol  tetranitrate,  and  10  minims  of 
tincture  of  digitalis  and  tincture  of  squills :  as  he  was  not 
asleep,  the  erythrol,  digitalis,  and  squill  were  repeated  at  5  p.m.  ; 
at  6.45  he  was  asleep,  and  slept  all  night.  On  the  9th  he 
was  still  very  tremulous,  but  the  mental  condition  had  im- 
proved ;  his  radials  were  decidedly  softer,  but  the  pressure 
was  150.  He  had  3  doses  of  the  medicines  last  mentioned 
during  the  day.  10th  January — slept  all  night;  mental 
condition  quite  clear:  arteries  soft,  pressure  120.  The 
erythrol  was  stopped  but  the  digitalis  and  squill  continued. 
12th  January — the  patient  had  completely  recovered;  the 
pressure  was  115,  the  radial  arteries  relaxed  and  soft.  On 
the  day  of  admission,  when  the  arteries  were  so  tightened  up 
that  they  felt  like  whipcord,  the  pressure  cannot  have  been 
less  than  180;  but,  owing  to  the  patient's  condition,  it  was 
quite  impossible  to  take  a  reading. 

Case  21. — J.  H.,  male,  aged  48,  was  admitted  by  a 
house  physician  on  11th  January  1907  to  Ward  3,  suffering 
from  delirium  tremens;  he  was  tremulous,  and  had  hallu- 
cinations of  vision.  The  patient  had  been  drinking  heavily 
for  some  time.  He  was  admitted  at  5  a.m.  I  saw  him  in 
the  forenoon,  and  found  his  pressure  at  11.30  was  150,  the 
pulse  was  96,  the  radial  artery  large  and  well  filled,  with 
a  thick  wall  and  a  large  wave.  He  was  given  i  grain  of 
erythrol  with  10  minims  each  of  tinct.  digitahs  and  tinct. 
scillffi  at  noon;  at  12.45  the  pressure  was  130.  At  6.20 
p.m.  the  pressure  was  140,  at  6.30  the  erythrol,  digitalis,  and 
squill  were  repeated,  and  at  8  the  pressure  was  130.  At 
11  o'clock,  as  he  was  excited  and  restless,  he  was  o-iven  20 
grains  of  trional;  at  11.45  he  was  asleep,  and  slept  until 
5  o'clock  the  following  morning.  On  12th  January,  at 
11.30~;a.m.  the  pressure  was  125;  on  13th  January,  at 
12.30  p.m.  it  was  125;  on  15th  January,  at  1.20  p.m.  it 
was  125;  and  on  17th  January,  at  12.30  p.m.  it  was  125. 
The    relaxation    and    softening    of    the    vessel    wall    which 

ii6 


ACUTE  ALCOHOLISM 

accompanied  the  fall  in  the  h^emonianometer  readings  were 
quite  perceptible  to  the  finger.  In  this  patient,  who  in 
ordinary  circumstances  would  have  had  a  day  or  two  of 
acute  delirium  tremens,  the  attack  was  aborted  by -a  single 
20-grain  dose  of  trional  given  after  his  vessels  were  relaxed 
by  erythrol. 

Case  22. — D.  F.,  male,  aged  49,  was  admitted  on  14th 
January  1907  to  Ward  3.  This  man  came  to  the  ward 
of  his  own  accord,  and  sought  admission  as  he  knew  he  was 
to  have  an  attack  of  dehrium  tremens.  He  had  been  in  the 
ward  on  several  previous  occasions.  He  j^i'esented  himself 
in  the '  period  of  abnormal  calm  which  in  him  was  known 
to  precede  the  alcoholic  storm.  It  was  not  until  the  I7th 
that  he  showed  any  cerebral  symptoms :  he  then  began  to 
hold  conversations  with  imaginary  people,  and  between  then 
and  the  18  th  he  became  wildly  restless  and  delirious. 
Erythrol  and  trional  combined  had  no  effect  upon  him,  but 
four  20-grain  doses  of  chloral  put  him  asleep  between  the 
18th  and  the  19th;  and  by  12.30  p.m.  on  the  19th  he  was 
awake  perfectly  sensible,  and  remained  so.  On  former 
occasions  much  more  chloral  had  been  used,  and  the 
duration  of  the  delirium  had  been  longer.  The  pressure 
on  the  loth  was  155:  on  the  17th,  140;  on  the  19th, 
140  ;  and  this  notwithstanding  several  -r-grain  doses  of 
erythrol.  On  the  29th  it  had  fallen  to  125,  the  pulse  was 
68,  the  vessel  soft  and  compressible.  On  the  15th,  the  day 
after  admission,  the  frequency  of  the  pulse  varied  from 
85  to  105,  and  the  vessel  wall  was  thick  and  contracted. 
The  influence  of  the  erythrol  was  very  striking  in  this  case, 
for  on  no  previous  occasion  had  his  delirium  been  so  cut  short, 
and  convalescence  been  so  rapid.  Chloral  acted  better  than 
trional  v/ith  this  patient.  The  reduction  of  pressure  from 
140  mm.  Hg.  to  125  was  effected  by  means  of  iodide  of 
potassium,  and  corresponded  with  the  complete  relaxation 
of  the  radial  artery.  This,  indeed,  was  a  case  in  which  I 
thought  there  must  be  permanent  thickening,  and  the  very 
definite  effect  of  the  iodide  was  a  surprise  to  myself. 

Case  23. — G.  H.,  male,  aged  31,  admitted  on  15th  March 

117 


H.EMOMANOMETER  PRESSURES 

1907  to  Ward  3,  having  drunk  heavily  and  having  taken  a 
"  fit."  On  admission  he  was  tremulous  and  nervous — the 
radial  artery  was  small  and  hard,  the  pressure  was  150. 
At  11.45  a.m.  he  was  given  erythrol  gr.  h  and  trional 
gr.  XX,  but  as  he  vomited  ten  minutes  after  they  were 
taken,  the  dose  was  repeated  at  3  p.m.  At  4.15  p.m.  he 
was  asleep,  and  slept  almost  continuously  till  5.30  the 
following  morning.  In  the  forenoon  the  pressure  was  130, 
the  radials  were  relaxed,  and  the  pulse  wave  larger.  This 
patient  was  practically  well,  and  went  out  on  the  18th. 

These  cases  wdien  arranged  as  below  show  how  naturally 
they  fall  into  two  groups ;  while  the  fall  in  pressure  in  each 
member  of  the  two  groups  is  seen  at  a  glance. 


Group  I. — Low  Pressures. 


Male,  aged  36. 

115 

mm.  Hg.  fell  to  95  mm.  Hg.  = 

=  fanof  20  mm.  ] 

,,       ,,     33. 

120 

,,     110 

,,     10 

,,       ,,     30. 

120 

,,     105 

,,     15 

,,     44. 

135 

,,     105 

,,     30 

„       ,,     38. 

115 

,,       95 

„     20 

,,       ,,     50. 

115 

.-,     100 
Ave'-age  fall,  18 '3  mm.  Hg. 

Group  II. — High  Pressures. 

,,     15 

Male,  aged  46. 

150 

mm.  Hg.  fell  to  115  mm.  Hg. 

—  fall  of  35  mm. 

,,       „     48. 

150 

„     125 

„     25         , 

,,       ,,     49. 

155 

„     125 

,,     30 

„       „     31. 

150 

„     130 

,,     20 

Hg. 


Average  fall,  27  "5  mm.  Ht 


ri8 


CHAPTER  XIV 

GROUPS  OF  CASES  ILLUSTRATING  H.EMO- 
MANOMETER  READINGS 

1.  FOUR    CONVALESCENTS    FROM    ACUTE    BRIGHT  ; 

2.  SEVEN    MISCELLANEOUS    CASES  ; 

3.  THIRTEEN    ELDERLY    AND    AGED    PERSONS  :    THE   RELATION 

BETWEEN    THE    RADIAL    AND    BRACHIAL    ARTERIES  ; 

4.  EIGHT    CASES  WITH    HEART    SYMPTOMS  :    THE    IMPORTANCE 

OF    RECOGNISING    HYPERTONUS    IN    CARDIAC    CASES. 

CONVALESCENTS  FEOM  ACUTE  NEPHRITIS. 

This  series  of  cases  illustrative  of  hsemomanometer  readings 
may  be  begun  with  the  following  4  cases,  in  which  there 
was  a  definite  diagnosis  of  acnte  Bright's  disease,  the  patients 
having  been  admitted  into  hospital  with  oedema,  and  albumin, 
blood,  and  casts  in  the  urine. 


Pressure. 

Case. 

Age  and  Sex. 

Disease. 

Condition  of 
Vessel  Wall. 

Oliver. 

Gartner. 

Mm.  Hg. 

Mm.  Hg. 

Cask  24 

Male,  aged  62 

Acute  Bright  ; 
convalescing 

Thickened  and 
sclerosed 

165 

150 

,,     25 

„     44 

Do.  improved 

Do. 

150 

130 

,,     26 

„     40 

Do.        do. 

Slight  thicken- 

130 

100 

„     27 

))         ))       9 

Do.   convalesc- 
ing 

ing 
No  sclerosis 

110 

Of  these  the  two  first  had  thickened  and  sclerosed  vessels, 
but  not  nearly  so  thick  as  were  the  vessels  in  the  series  of 

119 


ILLUSTRATING  HiEMOMANOMETER  READINGS 

kidney  cases  in  Chapter  XI. ;  in  the  third,  the  arteries  were  but 
slightly  thickened  ;  while  in  the  fourth,  a  boy  of  9  years  of 
age,  there  was  no  sclerosis.  The  state  of  the  arterial  wall 
corresponded  therefore  with  the  manometer  readings.  It 
will  also  be  observed  that  from  the  age  of  the  individuals 
no  definite  inference  can  be  drawn,  for  while  there  was  a 
pressure  difference  of  15  between  the  ages  of  62  and  44, 
there  was  a  difference  of  20  between  40  and  44,  and  a  like 
difference  of  20  between  the  ages  of  9  and  40.  The  factor 
of  age  will  be  dealt  with  more  fully  later. 

SEVEN  PATIENTS  UNDER  OBSERVATION  AT  THE  SAME 
TIME  :  PRESSURE  CORRESPONDING  WITH  THICK- 
NESS   OF   ARTERIAL   WALL. 

The  following  list  comprises  seven  patients  who  were  under 
observation  at  the  same  time  as  hospital  patients : — 


Pressure. 

Case. 

Age  and  Sex. 

Di.sease. 

Condition  of 
Vessel  Wall. 

Oliver. 

Gartner. 

1 
1 

Mm.  Hg. 

Mm.  Hg.' 

Case  28 

Male,  aged  37 

Brewery  worker 
for    20    years. 
Vertigo  ;      no 
alb. 

Thick    hard 

vessel 

170 

150 

„  29 

„     50 

Cabman,     con- 
valescent from 
jaundice  ;    no 
alb. 

Tliiok  vessel 

165 

159 

,,  30 

„         „     69 

Hydrothorax, 
etc.  ;  alb. 

Slight      vessel 
thickening 

135 

113 

„   31 

,,     64 

Aortic       and 
mitral  systolic 
murmurs 

Vessel  a  little 
thick  ;     com- 
pressible 

135 

i 

,,   32 

,,     55 

Antemia,    etc.  ; 
no  alb. 

Slight      vessel 
thickening 

.    125 

80       ! 

,,   33 

,,     40 

Sciatica,     been 
resting   for    6 
weeks;      no 
alb. 

Soft  vessel 

110 

90 

„  34 

,,     26 

Muscular  rheu- 
matism ;  alb. 

Soft  vessel 

105 

70 

These  cases  illustrate  the  general  rule — namely,  that  if 

I20 


A  GROUP  OF  ELDERLY  AND  AGED  PERSONS 

you  take  the  patients  in  a  hospital  ward,  the  manometer 
readings  will  be  found  to  closely  correspond  with  the  state  of 
the  radial  wall.  Any  other  group  of  persons  will  give  a  cor- 
responding result. 

In  Case  28,  the  brewery  worker,  observations  were  made 
after  he  had  been  for  a  week  on  spirit  of  nitrous  ether  and  a 
nightly  laxative.  His  vertigo  under  this  treatment  was 
cured,  and  he  was  feeling  well.  The  radial  artery  was  not 
quite  so  hard  as  it  had  been,  but  it  was  still  much  thickened, 
and  a  further  week  of  treatment  did  not  reduce  the  man- 
ometer reading.  In  fact,  this  man  had  at  the  age  of  37 
permanently  thickened  arteries,  due,  no  doubt,  to  20  years 
of  steady  beer-drinking. 

In  Case  29,  a  cabman,  the  observation  given  was  made 

A  GROUP  OF  ELDERLY  AND  AGED  PERSONS. 


Case. 

Age  and  Sex. 

Oliver. 

Condition  of 
Radial. 

Condition  of 
Fatient. 

Mm.  Hg. 

Case  35 

Mrs.  C,  Q.H.,aged68    . 

260 

Thick     and 
hard 

Engaged    in 
house  work 

„    36 

J.  F.,  male,  Q.H.,  aged  72     . 

240 

Thick  artery 

Has  had  hemi- 

„    37 

R.  C,  male,  Q.H.,  aged  72     . 

235 

Thick     and 

paresis 
Supra-pubic 

„    38 

A.S.,  male,  Q.H.,  aged  58      . 

200 

hard 
Thick 

cystotomy 
Old     h  e  m  i- 

,,    39 

G.  G.,  female,  Q.H.,  aged  69  . 

200 

Hard,  ather- 
0  ma  to  us 
and   cal- 
careous 

paresis 
Demented 

„    40 

Mrs.  R.,  Q.H.,  aged  92  . 

170 

Soft     and 
small  vessel 

Has  all  her 
faculties,  and 
out  of  bed 
daily 

Confined       to 

„    41 

Mrs.  B.,  Q.H.,  aged 

155 

Cordy     and 

tortuous 

bed 

„     42 

Mrs.  R.,  private,  aged  80 

160 

Some  thick- 
ening 

Fairly  active 

,,     43 

Mrs.  S.,  private,  aged  82 

160 

Thick 

Do. 

,,     44 

Mrs.  J.,  Q.H.,  aged  64  . 

140 

Soft 

Secondary 
anaemia    from 
malignant 
disease 

,,     45 

Mrs.  H.,  private,  aged  70 

130 

Soft      and 

Good  health 

„     46 

Mrs.  L,  private,  aged  70 

125 

compressible 
Do. 

Fairly  vigorous 

„    47 

Mrs.  M.,  private,  aged  69 

120 

Do. 

Do. 

121 


ILLUSTRATING  HiEMOMANOMETER  READINGS 

after  he  had  had  pilocarpine,  and  indicated  the  irreducible 
minimum  below  which  no  reduction  of  manometer  reading 
would  be  obtained,  because  of  the  degree  of  permanent 
thickening  in  the  vessels. 

The  age  of  the  patients  in  this  group  also  has  no  fixed 
relation  to  the  manometer  readings.  The  highest  reading 
was  from  a  man  of  37,  one  of  the  lowest  from  a  man  of  40. 
In  the  two  patients  with  readings  of  110  and  105  the  vessel 
wall  was  soft  and  unthickened.  The  intermediate  cases  with 
readings  of  125  and  135  showed  some  thickening  of  the 
vessel,  whether  permanent  or  merely  due  to  hypertonic 
contraction  is  immaterial  so  far  as  the  conclusions  drawn 
from  the  readings  are  concerned. 

See  Talk  on  p.  121. 

The  cases  on  p.  121  show  in  the  first  place  how  erroneous 
is  the  idea  that  blood-pressure  rises  with  age ;  and  secondly, 
that  if  vessels  are  thick,  hcfimomanometer  readings  are  high ; 
if  not  thickened,  they  are  normal. 

The  Relation  between  the  Radial  and  Brachial 
Arteries. — Such  readings  could  of  course  be  multiplied  almost 
indefinitely,  but  I  do  not  think  this  would  serve  any  useful 
purpose.  That  the  readings  represent  anything  like  the  varia- 
tions in  blood-pressure  which  the  figures  show,  I  can  hardly 
imagine  anyone  with  a  cultivated  knowledge  of  the  pulse  main- 
taining. The  pressures  corresponded,  not  with  blood-pressure  as 
perceived  through  the  cultivated  finger,  but  with  the  palpable 
measure  of  thickening  or  hardness  of  the  radial  artery  at 
the  wrist.  There  are,  however,  occasional  cases  where  this 
proposition  does  not  hold.  Sometimes  a  patient  with  a  thick 
radial  gives  a  moderate  degree  of  pressure,  as  in  Case  41, 
where  with  a  cordy  radial  the  pressure  was  only  155:  in 
some  other  cases,  with  a  soft  and  compressible  radial,  the 
pressure  is  relatively  high,  as  in  Case  44,  where  with  a  soft 
pulse  in  advanced  debility  from  malignant  disease  the 
pressure  was  144.  I  have  not  found  that  the  plumpness  or 
leanness  of  the  upper  arm  materially  influences  the  readings. 
So  far  as  I  can  see,  the  explanation  is  to  be  found  by 
assuming  that  the  condition  of  the  wall  of  the  brachial  artery, 
which  of  course  is  the  vessel  compressed,  does  not  correspond 

122 


RELATION  OF  RADIAL  AND  BRACHIAL  ARTERIES 

with  that  of  the  radial  as  revealed  by  manipulation. 
h)upport  is  given  to  this  as  the  probable  explanation  by  the 
fact  that  occasionally  one  finds  that  the  radial  artery  at  the 
wrist  may  be  distinctly  softer  than  it  is  in  the  middle  of 
the  forearm.  The  general  proposition  that  the  pressure  will 
Ije  found  to  closely  correspond  with  the  condition  of  the  radial 
wall,  will  however  be  found  to  be  sound.  So  definitely  is  this 
the  case  that  in  many  instances  the  pressure  can  be  approxi- 
mately guessed,  after  some  experience,  while  at  the  same 
time  it  must  be  recognised  that  it  is  not  wise  to  be  over- 
confident. The  position  may  be  restated  as  follows :  It  is 
to  the  upper  arm  that  the  compression  bag  is  applied,  and 
when  the  pulse  at  the  wrist  stops,  it  is  owing  to  the 
obliteration  of  the  flow  in  the  brachial  artery.  The  wall  of 
the  brachial  artery  varies  in  thickness  as  the  result  of 
sclerosis,  of  atheroma,  and  of  hypertonic  contraction.  The 
variations  in  its  thickness  determine  the  amount  of  pressure 
necessary  to  compress  it  so  as  to  arrest  the  radial  pulse. 
In  the  great  majority  of  cases  the  amount  of  pressure 
necessary  to  obliterate  the  brachial  can  be  judged  of  by 
the  thickness  of  the  radial  artery  ;  but,  in  a  small  number 
of  cases,  these  do  not  correspond,  and  the  only  possible 
explanation  is  that  the  radial  is  not  in  them  a  reliable 
index  of  the  condition  of  the  brachial  artery.  The  second 
case  (Case  36)  in  the  preceding  list  is  an  example  of 
this.  He  had  a  moderately  thick  radial  artery  with 
moderate  pressure  in  it,  so  that  I  thought  it  was  hardly 
necessary  to  take  his  pressure.  I  did  so,  however,  as  I 
intended  giving  erythrol  tetranitrate  on  account  of  the 
recurrence  of  a  slight  right  hemiparesis,  and  it  was  much  to 
my  surprise  to  find  that  the  obliterating  pressure  was  as 
high  as  240—250,  and  that  it  remained  at  that  after  days 
of  erythrol.  The  erythrol  seemed  to  distinctly  improve  his 
condition,  although  his  brachial  pressure  remained  the  same. 
This  man's  brachial  artery  felt  hard  and  difficult  to  compress 
by  the  fingers ;  but  I  state  this  with  reserve,  for  I  have  not 
yet  studied  the  brachial  artery  sufficiently  to  have  confidence 
in  the  value  of  observations  made  by  my  fingers.  The 
brachial  is,  as  a  matter  of  fact,  much  more  difficult  to  gauo;e 
by  the  finger  than  the  radial,  as  anyone  can  prove  by  trying 

123 


ILLUSTRATING  HvEMOMANOMETER  READINGS 

it.      The    following   is    a    spliygmograpbic    tracing  from  this 
man's  radial  artery  : — 

Since  the  above  was  written  further  developments  have 
occurred  which  are  worthy  of  note.      On  the  6th  of  September 


Fig.  31. — Tracing  from  Case  .36.     Hremomanometer  Pressure,  200  mm.  Hg. 

the  patient  developed  left  hemiparesis,  and  I  had  him  trans- 
ferred to  my  ward  in  the  Infirmary.  On  admission  his  pres- 
sure was  found  to  be  240  mm.  Hg. ;  under  erythrol  it  fell  to  220 
mm.  Hg:  The  condition  of  the  radial  artery  did  not  suggest 
a  pressure  over  160  mm.  Hg.  On  again  carefully  palpating 
the  'brachial  artery  it  was  felt  to  be  very  thick-walled  and 
tortuous,  this  condition  of  the  artery  being  both  felt  and  seen 
at  the  bend  of  the  elbow.  It  was  as  easily  appreciated  by 
others  as  by  myself.  I  find  that  the  best  way  of  palpating 
the  brachial  artery  is  to  pass  the  fingers  round  the  back  of 
the  arm  to  its  inner  side,  the  observer  using  the  left  hand  for 
the  patient's  right  arm  as  he  stands  on  the  patient's  right 
side.  In  the  upper  third  of  the  arm  the  vessel  can  as  a  rule 
]3e  readily  felt  and  the  condition  of  its  wall  estimated.  In 
this  case  there  was  a  difference  of  30  mm.  Hg.  between  the 
obliterating  pressure  in  the  upper  and  lower  arm. 

This  want  of  relation  between  the  radial  pulse  and  the 
compressibility  of  the  brachial  artery  as  measured  by  the 
hoemomanometer  has  no  doubt  been  the  source  of  the  pro- 
position that  the  finger  is  an  unreliable  test  of  blood-pressure. 
It  is  a  comfort  to  think  that  the  use  of  the  finger  is  not  yet 
obsolete,  and  that  the  claim  of  the  htemomanometer  to  a 
more  modest  place  may  the  more  easily  establish  its  true 
value  as  a  clinical  instrument. 

EIGHT   CASES   WITH   HEART    SYMPTOMS. 
In  this  series  of  cases  the  same  proposition  holds- — namely, 

124 


CASES  WITH  HEART  SYMPTOMS 


that  the  htemomanometer  readings  correspond  closely  with 
the  condition  of  the  arterial  wall.  The  most  striking  example 
is  in  Case  54  :  the  patient  was  an  old  man  brought  in  a  state 
of  collapse  to  my  ward  in  the  Infirmary  by  the  police.  He 
rallied  under  judicious  stimulation  administered  by  the  house 
physician.  His  arteries  were  thick  and  hooped,  with  any- 
thing but  a  vigorous  wave  inside  them,  and  yet  four  days 
after  admission  his  heemomanometer  pressure  was  210.  At 
the  other  extreme  is  a  man  of  63  with  a  soft  compressible 
artery  and  a  htemomanometer  pressure  of  95  only.  I  doubt 
if  there  were  20  mm.  Hg.  between  the  real  pressures  in  these 
two  cases,  and  yet  the  haemomanometer  gave  a  difference  of 
115  mm.  Ho;.  ' 


Case. 

Sex  and  Age. 

Condition  of  Radial  Artery. 

Oliver. 

Mm.  Hg. 

Case  48 

Male,  aged  64 

Artery  a  little  thick  (angina  pectoris) 

135 

„    49 

,,     64 

Artery  thick  (double  mitral) 

160 

,,    50 

,,     57 

Small — thready  (double  mitral) 

120 

,,    51 

„      41 

Arterv  thick  (double  aortic) 

145 

,,    52 

,,     59 

Slight  thickening  (double  aortic) 

125 

,,    53 

,,     46 

Do.         (mitral  and  aortic  systolic) 

125 

,,   54 

,,             aged 

Thick  and  hooped  (4  days  after  collapse 
from  heart  failure,  alb. ) 

210 

,,   55 

„         „     6.3 

Soft  compressible  artery — feeble  heart — 
splenic  leuktemia 

95 

With  regard  to  the  other  cases,  five  of  which  were  under 
treatment  for  symptoms  referable  to  valvular  lesion,  the 
condition  of  the  artery  is  seen  to  correspond  with  the  htemo- 
manometer  readings. 

The  Importance  of  recognising  Hypertonus  in  Heart- 
Cases. — It  is  desirable  not  to  pass  from  this  group  of  cases 
without  drawing  attention  to  the  very  great  importance  of 
recognising  hypertonus  in  heart  cases.  There  is  nothing  about 
it  in  literature,  so  far  as  I  have  seen.  Sir  James  Barr  has 
looked  at  the  circulation  from  the  periphery.  Professor 
Saundby  in  a  recent  clinical  lecture  definitely  refers  to  the 
value  in  some  cases  of  heart  disease  of  dilating  the  peripheral 
vessels.  It  is  a  fact  which  has  been  long  known  to  me,  and 
which  I  have  used  with  much  success.  That  the  fact  has 
not  been  more  widely  recognised  is  the  result  of  the  idea  of 

125 


ILLUSTRATING  H.EMOMANOMETER  READINGS 

"  peripheral  obstruction "  having  been  largely  outside  the 
"  working  principles  "  of  daily  practice.  When  it  is  properly 
recot£nised  it  will  be  often  found  that  what  a  heart  needs  is 
not  to  be  lashed  l^y  cardiac  tonics,  but  to  have  measures  taken 
for  the  relief  of  the  hypertonic  contraction  of  peripheral  vessels, 
with  its  corresponding  lowering  of  aortic  blood-pressure.  In 
heart  as  in  other  conditions  the  relaxation  of  hypertonus 
makes  the  arterial  w^all  thinner,  and  there  is  a  fall  in  heemo- 
manometer  reading.  Let  me  again  warn  those  interested  that 
relaxing  treatment  must  not  be  adopted  merely  on  the  strength 
of  hsemomanometer  readings.  A  thick  vessel  with  a  correspond- 
ing low  reading,  say  of  135,  may  require  to  have  its  tone  raised  ; 
while  a  thinner- walled  vessel,  with  say  a  reading  of  125,  may 
with  advantage  have  its  tone  lowered  slightly.  The  element  of 
cultivated  skill  cannot  be  eliminated.  The  internal  pressure, 
and  the  relation  of  the  vessel  wall  to  its  contained  blood, 
have  to  be  judged  of ;  and  the  daily  hsemomanometer-reading 
merely  helps  the  finger  in  the  determination  of  the  therapeutic 
course  to  be  taken  day  by  day. 

REFERENCES. 

T.  Clifford  Allbutt,  Rise  of  Blood-pressure  in  Later  Life,  Med. 
Chi.  Trans.,  vol.  86.  Saundby,  Brit.  Med.  Journ.,  1906,  vol.  ii. 
p.  98.5.  Sir  James  Barr,  Address  at  Montreal,  Brit.  Med.  Journ., 
1906,  vol.  ii.  p.  401. 


1 :0 


CHAPTER   XV 

THE  RELATION  OF  ANGINA  PECTORIS  AND 
ALLIED  CONDITIONS  TO  AN  ARTERIO- 
CARDIAC  REFLEX  HAVING  ITS  ORIGIN  IN 
THE  ABDOMEN,  AND  CAUSING  HYPERTONIC 
CONTRACTION  ^ 

Introductoey. — Angina  pectoris  has  attracted  the  attention, 
and  at  times  riveted  the  thought,  of  many  clinicians  during 
the  past  one  hundred  and  thirty  years.  That  it  should  still 
exercise  the  same  influence  over  the  clinicians  of  to-day  need 
not,  therefore,  cause  surprise.  Gibson  of  Edinburgh,  Oliver 
of  Newcastle-upon-Tyne,  and  Mackenzie  of  Burnley  have  all 
three  recently  shown  that  they  were  the  victims  of  the 
fascination  or  attractiveness  of  the  subject.  The  views  which 
are  submitted  here  have  emerged  from  the  special  attention 
which  I  have  long;  given  to  cardiac  and  vascular  disturbances, 
and  more  recently  from  a  fuller  knowledge  of  the  processes  of 
primary  and  secondary  digestion,  of  nutrition,  and  of  elimina- 
tion. My  indebtedness  to  the  work  of  Pawlow,  Herter, 
Chittenden,  and  others  I  gratefully  acknowledge.  Instead  of 
conflicting  with  past  observations,  these  views  interpret  them, 
and  give  the  clue  to  the  disentanglement  of  the  confused 
mass  of  opinion  on  the  subject. 

Historical — Helerden  to  Trousseau,  1768-1862. — AVe  do 
not  require  to  go  farther  back  in  our  historical  retrospect 
than  the  date  when  the  term  "  angina  pectoris "  was  in- 
troduced into  medical  nomenclature.  Those  who  wish  to 
examine  the  earliest  records  of  the  symptoms  called  by  this 
name  will  find  the  references  in  several  of  the  older  authors, 
particularly  in  Parry's  monograph. 

^  This  chapter  is  the  reproduction  of  a  paper,  with  some  alterations,  Avhich 
was  published  in  the  British  Medical  Journal,  10th  February  1906. 

127 


ANGINA  PECTORIS 

Angina  pectoris  was  the  name  given  by  William  Heberden, 
in  the  year  1768,  to  a  disorder  of  the  breast,  which  he  thus 
described :  "  Those  who  are  affected  with  it  are  seized  while 
they  are  walking,  and  more  particularly  when  they  walk  soon 
after  eating,  with  a  painful  and  most  disagreeable  sensation  in 
the  breast,  which  seems  as  if  it  would  take  their  life  away  if 
it  were  to  increase  or  to  continue."  "  The  seat  of  it  and  sense 
of  strangling  and  anxiety  with  which  it  is  attended  may  make 
it  not  improperly  be  called  angina  pectoris." 

As  regards  the  nature  of  the  disease  to  which  he  gave 
this  name,  he  says  that  "  the  opinion  of  its  being  a  convulsion 
of  the  part  affected  will  readily  present  itself  to  anyone " 
(p.  64). 

In  a  later  paper,  of  date  1785,  containing  the  account  of 
the  'jjost-mortem  examination  on  the  historical  "  unknown,"  he 
reports  that  there  was  no  lesion  found ;  and  in  his  comments 
on  treatment  he  advocated  the  use  of  medicines  which 
"relieve  and  quiet  convulsive  motions"  (vol.  iii.  p.  10). 

Here  at  the  fountain-head  is  found  the  idea  of  the 
nervous  nature  of  the  clinical  phenomena  of  angina  pectoris, 
a  conception  of  the  condition  shared  by  many  subsequent 
writers. 

The  next  step  worthy  of  note  was  made  by  Dr.  Caleb 
Hillier  Parry,  a  physician  in  Bath,  who  published  in  1799  a 
monograph  entitled  An  Inquiry  into  the  Symptoms  and  Causes 
of  the  Syncope  Anginosa,  commonly  called  Angina  Pectoris. 
This  work  is  characterised  by  remarkable  clinical  acumen, 
and  Parry's  views,  it  seems  to  me,  have  not  always  been 
accurately  presented  by  subsequent  writers.  Some  of  the 
clinical  points  dealt  with  by  him  are  to  be  specially  noted. 
He  points  out,  for  instance,  that  the  first  symptom  is  "  an 
uneasy  sensation  (described  variously  as  a  stricture,  an 
anxiety,  or  a  pain)  about  the  middle  of  the  sternum,  across 
the  left  breast,  and  in  certain  stages  of  the  disorder  usually 
stretching  into  the  left  arm"  (p.  42),  also  that  the  pain  occurs 
in  paroxysms,  and  that  early  seizures  seldom  occurred 
without  apparent  cause  (p.  43).  He  also  insists,  "  we  shall 
always  find  it  (the  pulse)  become  more  or  less  feeble 
according  to  the  violence  of  the  paroxysm"  (p.  45).  Here 
we   have  an    early   recognition  of    great  differences    in    the 

128 


ANGINA  PECTORIS 

degree  of  severity  in  the  leading  syrDptom.  The  pathology 
of  the  condition  was  held  by  him,  and  by  his  friend  Jenner, 
to  be  disease  of  the  coronary  arteries  interfering  ^vith  the 
blood  supply  to  the  heart.  His  induction  was  that  a  heart 
with  such  coronary  arteries  could  not  bear  any  extra 
strain  put  upon  it ;  that  if  subjected  to  extra  strain  it 
became  surcharged  with  blood ;  that  its  action  became 
enfeebled,  and  might  cease.  The  extra  strain  could  be 
induced  by  mental  emotion,  by  physical  effort,  and  by  gastro- 
intestinal conditions.  As  the  heart  condition  advanced,  even 
slighter  causes  than  these  might  produce  paroxysms.  Thus 
heart  failure  and  its  organic  cause  formed  the  central,  and 
to  him  the  essential,  factors,  in  determining  the  gravity  of 
the  condition.  According  to  Cullen's  nosology,  this  was  as- 
suredly a  syncope.  "  The  motion  of  the  heart  diminished,  or 
even  for  some  time  ceasing.  Motus  cordis  immiiiutus,  vel 
aliquamdhc  quiescens."  It  differed  from  an  ordinary  syncope 
"  only  in  being  preceded  by  an  unusual  degree  of  anxiety  or 
pain  in  the  region  of  the  heart."  He  therefore  termed  the 
disorder  sT/ncojje  anginosa.  To  make  the  position  of  this  old 
Bath  physician  still  more  clear,  let  me  give  his  own  words 
regarding  a  patient  who  had  been  long  subject  to  attacks 
of  what  he  considered  a  "  very  pure  angina  pectoris.'"'  He 
accompanied  his  patient  on  a  walk  uphill  in  order  to 
witness  what  occurred  during  the  fit.  He  says,  "  When  the 
paroxysm  was  thus  excited,  I  could  perceive  no  symptom  of 
disorder  in  addition  to  the  uneasiness  in  the  breast,  except  a 
gradual  and  most  evident  diminution  in  the  strength  of  the 
pulse"  (p.  59). 

Allan  Burns,  Professor  of  Anatomy  and  Surgery  in 
Glasgow,  and  practising  in  that  city  (1809),  accepts  Parry's 
view  that  syncope  anginosa  orginates  "  from  some  organic 
lesion  of  the  nutrient  vessels  of  the  heart"  (p.  137).  He 
compares  a  heart  with  "  cartilaginous  or  ossified "  .coronary 
vessels  to  a  limb  with  a  ligature  round  it  called  into  active 
exercise.  The  limb  so  bound  can  only  work  for  a  very  short 
time ;  "  it  soon  fails  and  sinks  into  a  state  of  quiescence  "  (p. 
138).  He  holds  that  "the  essence  of  this  complaint  consists 
in  a  reduction  of  the  action  of  the  heart"  (p.  1-46). 

In  1815,  Jurine,  in  an  essay  to  which  the  Academy  of 
I  129 


ANGINA  PECTORIS 

Medicine  awarded  a  medal,  combated  Jenner's  and  Parry's 
view  that  angina  pectoris  was  due  to  ossification  of  the 
coronary  arteries.  To  him  "  sans  douleur  sternale,  il  n'y  a 
pas  d'angine  de  poitrine "  (p.  72),  and  he  argued  that  the 
angina  was  essentially  due  to  an  affection  of  the  pulmonary 
nerves  (p.  123). 

Laennec,  (1819),  had  found  that  in  several  subjects 
who  had  laboured  under  angina  pectoris,  and  in  whom  there 
co-existed  either  hypertrophy  or  dilatation  of  the  heart,  there 
was  no  ossification  of  the  coronary  arteries  (p.  757). 
According  to  him,  "  angina  pectoris  in  a  slight  or  middling 
degree  is  extremely  common,  and  exists  very  frequently  in 
persons  who  have  no  organic  affection  of  the  heart  or  large 
vessels"  (p.  756).  Desportes  (1811)  is  quoted  by  Laennec 
as  holding  similar  views.  Angina  pectoris  was  to  Laennec  a 
neuralgia. 

Forbes  (1832),  the  translator  into  English  of  Laennec's 
great  work,  divided  cases  of  angina  pectoris  into  organic  and 
functional.  The  pain  to  him  was  the  result  of  "some 
unknown  temporary  condition  of  the  nerves  of  the  part,"  and 
he  believed  that  "  such  a  morbid  condition  of  the  nerves  may 
be  produced  in  a  heart  in  all  other  respects  sound." 

Bertin  (1833)  also  repudiated  the  view  that  angina 
pectoris  was  due  to  ossification  of  the  coronary  arteries. 
He  had  seen  the  symptoms  "  accompanied  with  a  multitude 
of  organic  affections,  either  of  the  heart  or  of  the  large 
vessels,  or  even  of  the  lungs"  (p.   410). 

Hope  (1839)  held  that  "the  nature  and  variability  of 
the  symptoms  of  angina  pectoris  confirm  the  opinion  of 
Laennec  that  it  is  a  neuralgic  affection"  (p.   499). 

Latham  (1846),  along  with  a  vivid  portrayal  of  angina 
pectoris,  considered  the  disease  to  be  "  a  certain  assemblage 
of  symptoms,  and  not  any  constant  pathological  condition 
belonging  to  the  structure  of  the  organ"  (p.  399).  The 
paroxysm  was  to  him  "  plainly  a  compound  of  pain  and  of 
something  else"  (p.  385).  It  was  a  "  spasm  of  the  heart," 
as  it  had  been  to  Heberden.  But  then  note  his  conception 
of  spasm.  He  says :  "  Spasm  is  always  accompanied  with 
pain.  And  pain  and  spasm,  wherever  they  are,  disable  the" 
part  which  they  befall"  (p.   385).     "In  spasms  of  smaller 

ISO 


ANGINA  PECTORIS 

degree  the  heart  fails  to  close  freely  upon  the  blood  and  to 
impel  it  freely  into  the  arteries.  In  its  spasm  of  greater 
degree  it  fails  to  project  it  altogether"  (p.   386). 

Walshe  (1851)  looked  upon  angina  pectoris  as  a  "par- 
oxysmal neurosis  in  which  the  heart  is  essentially  concerned  " 
(p.  190).  He  thought  genuine  angina  pectoris  to  be  a  very 
rare  disease,  while  on  the  other  hand  he  "  very  frequently  met 
with  a  form  of  complaiut  combining  in  a  minor  degree  many 
of  the  characters  of  angina."  To  this  "  imitation  of  the  true 
disease  "  he  gave  the  name  of  "  pseudo-angina."  He  thought 
that  this  was  the  explanation  of  Laennec's  notion  that  the 
condition  was  of  very  frequent  occurrence  (p.   203—4). 

Stokes  (1854)  agreed  with  Parry,  and  says  "that  the 
symptoms  of  angina  arise  from  a  temporary  increase  of  weak- 
ness in  an  organ  already  weakened"  (p.  486).  He  disputes 
Latham's  idea  of  spasm,  and  thinks  the  idea  of  syncope  more 
in  accordance  with  observed  fact. 

Trousseau  refers  to  the  variety  of  pathological  change 
which  had  been  described  as  having  been  present  in  the 
hearts  of  persons  who  had  suffered  from  angina  pectoris.  On 
the  other  hand,  he  has  of  necessity  to  admit  that  angina 
pectoris,  even  when  most  intense,  need  not  ])e  a  symptom  of 
an  organic  lesion.  He  therefore  regarded  the  organic  changes, 
when  they  were  present,  as  non-essential,  as  coincidences,  and 
held  that  the  real  affection  was  a  neurosis — in  fact,  a  neuralgia. 
That  there  might  be  no  ambiguity  in  the  minds  of  his  hearers, 
he  again  repeated  his  opinion  that  it  might  be  only  "  an 
idiopathic  neuralgia." 

Three  Views. — At  this  point  we  may  draw  a  line  and 
say  that  up  to  it  there  were,  if  we  exclude  Jurine's  view 
— which  we  may  safely  do — three  views  regarding  angina 
pectoris  :  the  first,  that  it  was  a  convulsion  of  the  heart,  or  a 
spasm  of  it ;  the  second,  that  it  was  due  to  interference  with 
its  blood  supply ;  and  the  third,  that  it  was  a  neurosis — the 
word  having  no  su1)tle  or  obscure  significance,  but  meaning 
simply  and  plainly,  a  neuralgia — an  idiopathic  pain  in 
nerves.  Up  to  this  time,  it  is  also  important  to  note  that- 
the  new  term  was  not  limited  to  a  relatively  rare  malady, 
characterised  by  a  few  dramatic  incidents  and  a  suddenly' 
tragic   conclusion.       Its   use   had   become    so    extended    that 

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ANGINA  PECTORIS 

Walshe  deemed  it  desirable  to  introduce  the  term  pseudo- 
angina,  under  which  to  range  the  cases  that,  in  spite  of 
the  correspondence  in  symptoms,  had  not  the  grave  sig- 
nificance that  the  fatal  angina  of  Heberden  presented. 

Angina  Pectoris  Vasomotoria. — ^With  the  year  1867 
a  new  factor  was  introduced  into  the  discussion  on  the 
nature  of  angina  pectoris.  Nothnagel  in  that  year  wrote  a 
paper  which  he  entitled  Angina  Pectoris  Vasomotoria.  In 
this  condition  the  symptoms  closely  resembled  those  of  angina 
pectoris,  and  would  certainly,  I  think,  have  been  placed  under 
that  designation  by  some  of  the  distinguished  clinicians  whose 
works  have  been  referred  to.  The  essential  point  in  this 
paper  was  the  recognition  of  the  important  clinical  fact  that 
in  this  group  of  cases  narrowing  of  the  arteries  preceded 
and  caused  the  cardiac  embarrassment  and  other  symptoms ; 
that,  in  fact,  the  anginous  symptoms  were  secondary  to  the 
vasomotor  ones ;  and  that  by  relieving  the  cramp  in  the 
vessels  the  anginous  symptoms  were  prevented  coming  on. 

Earlier  Observations  on  Blood  Supply  and  Muscle 
Pain,  Intermittent  Claudication.  —  Before  Nothnagel, 
Latham,  when  dealing  with  the  treatment  of  persons  the 
victims  of  angina  pectoris,  had  not  failed  to  note  the  guidance 
to  be  obtained  from  a  true  estimate  of  the  condition  of  the 
vascular  system.      He  says  : 

"  The  paroxysm  is  often  put  off  and  its  severity  mitigated 
and  life  prolonged  by  no  means  more  surely  than  by  keeping 
the  vascular  system  in  a  just  balance  between  fulness  and 
emptiness,  between  rich  blood  and  poor  blood"  (p.  405). 

Three  years  before  the  date  of  the  publication  of  Latham's 
lectures,  Sir  Benjamin  C  Brodie's  Lectures  on  Pathology  and 
Surgery  were  published  (1846).  In  them  there  is  a  lecture 
on  senile  gangrene  which  I  doubt  if  any  living  surgeon  could 
add  to.  He  notes  that  the  condition  might  be  due  to 
ossification  of  arteries  or  to  obliteration  without  ossification. 
He  enlarges  upon  the  prodromal  symptoms  of  gangrene — he 
had  noted  the  numbness,  pain,  and  loss  of  muscular  power 
— which  may  precede  its  visible  manifestation.  With  the 
clinical  instinct  of  the  great  men  of  liis  time,  he  applied 
these  observations  to  interpret  the  much-discussed  question 
as    to   the  nature  and  causes    of  the   pain  in  angina.      The 

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ANGINA  PECTORIS 

paroxysm  of  pain  in  angina  varied  in  intensity,  so  it  did  in 
gangrene,  greatly.  The  pain  in  gangrene  might  become 
excruciating — the  pain  of  angina  might  fail  to  find  words 
adequate  to  convey  a  true  sense  of  its  anguish.  "  The 
disease,"  he  says,  "  is  called  neuralgia,  which,"  he  adds, 
"means  nothing"  (p.  356).  A  clear  thinker,  as  well  as  a 
masterly  observer,  this  surgeon  of  sixty  years  ago  ! 

A  still  earlier  recorded  observation  bearing  upon  the 
relation  between  lessened  blood  supply  and  pain  must  not  be 
omitted  were  it  only  for  the  sake  of  historical  accuracy.  At 
the  Academic  Eoyale  de  Medecine,  the  Seance  of  4th  October 
1831,  Boullay  submitted  an  observation  he  had  made 
on  a  mare  of  a  condition  to  which  he  gave  the  name 
of  "  intermittent  claudication."  The  symptoms  came  on 
abruptly  after  some  minutes'  exercise,  and  they  were  found 
to  be  due  to  obliteration  of  the  femoral  arteries.  When  the 
animal  was  in  repose  tlie  blood  was  able  to  reach  the  limbs 
by  the  collaterals,  but  when  it  trotted  the  compressed  col- 
laterals did  not  furnish  enough  blood,  and  the  limbs  were 
seized  by  cngourcUssement  and  by  severe  pain,  which  made  the 
animal  fall. 

Charcot,  twenty-six  years  later,  revived  this  subject,  and 
drew  attention  to  a  corresponding  condition  as  it  occurred 
in  the  limbs  in  man  as  causing  severe  pain,  and  as  a  pre- 
monitory sign  indicative  of  a  tendency  to  senile  gangrene. 
So  far  as  I  have  found,  he  did  not  apply  his  observations  to 
the  elucidation  of  the  symptoms  of  angina  pectoris  as  the 
English  surgeon  Brodie  had  done  ten  years  earlier. 

After  this,  however,  intermittent  claudication  as  a  cause 
of  painful  muscle  spasm  took  its  place  in  medical  literature, 
and  has  been  much  used  by  later  writers  when  discussing  the 
cause  of  the  pain  in  anginous  paroxysms. 

Arterial  Spasm. — Standing  alone,  and  forming  an  epoch 
by  itself,  is  Lauder  Brunton's  discovery  (1867)  that  dilata- 
tion of  the  peripheral  vessels  by  the  inhalation  of  nitrite  of 
amyl  removed  or  relieved  anginous  symptoms.  From  this 
date  vasomotor  spasm  became  a  still  more  definite  factor  in 
the  consideration  and  the  interpretation  of  the  "  syndrome  of 
symptoms  "  known  as  angina  pectoris. 

What  is  included  under  "  Angina  Pectoris  "  ? — What, 

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ANGINA  PECTORIS 

then,  are  we  to  regard,  as  angina  pectoris  ?  Are  we  to 
confine  the  use  of  the  term  to  that  type  of  case  described 
with  such  dramatic  force  by  some  of  the  earlier  writers  that 
there  still  lingers  round  its  earlier  records  a  glamour  of 
picturesqueness  ?  Are  its  symptoms  to  be  bounded  by  the 
dolor  pectoons  and  the  angor  animi.  of  its  early  recognition, 
and  is  its  close  to  be  characterised  by  the  same  tragic 
suddenness  ?  I  think  not.  From  the  time  of  Parry  the 
term  "  angina  pectoris "  has  been  applied  to  symptoms  of 
less  gravity,  and  to  conditions  where  the  outlook  was  not 
necessarily  grave.  Let  me  clinch  this  statement  by  quoting 
the  words  of  Professor  W.  T.  Gairdner,  who,  writing  in 
1877,  says:  "We  now  know  that  this  typical  angina  is  only 
the  culminating  form  of  a  group  of  symptoms,  which  in  their 
less  pronounced,  less  definitely  painful,  and  more  complicated 
forms,  are  found  to  permeate  the  whole  field  of  cardiac 
pathology  and  diagnosis  "  (p.  570). 

From  his  own  personal  experience  he  says :  "  There  is 
often  an  element  of  subjective  abnormal  sensation  present  in 
cardiac  diseases  which,  when  it  is  not  localised  through  the 
coincidence  of  pain,  is  a  specially  indefinable  and  undescrib- 
able  sensation"  (p.  5  65).  "A  sensation  which  can  only  be 
called  anxiety,  or  cardiac  oppression  "  (p.  566). 

To  this  group  of  symptoms  he  gave  the  special  title 
angina  sine  clolorc,  recognising  thereby  what  he  believed  to 
l3e  "  its  true  diagnostic  and  pathological  significance  and  its 
alliance  with  the  painful  angina  of  Heberden."  Even  the 
dolor  pectoris  is,  then,  no  longer  an  essential  symptom  ;  and 
the  angor  animi  is  whittled  down  to  a  sensation  of  anxiety. 
This  shrewd  clinical  pathologist  saw,  how^ever,  that  there 
were  phenomena  which,  while  different  to,  were  of  the  same 
kind  as  those  of  the  classical  angina.  This  is  what  Walshe 
recognised  when  he  used  the  much-abused  term  "  pseudo- 
angina."  While  Gairdner  places  angina  amongst  the 
neuroses,  he  hardly,  I  think,  attaches  the  same  meaning  to 
the  word  as  the  earlier  writers  did  :  and  I  am  not  sure  that 
he  does  not  somewhat  grudgingly  stick  to  the  term.  He 
was  clearly  impressed  by  the  possible  importance  of  vasomotor 
spasm. 

Dr.  Sansorn,  on  the  other  hand  (1892),  thinks  it  probable 

134 


ANGINA  PECTORIS 

that  a  paroxysm  of  angina  pectoris  is  an  intense  nerve  storm, 
provoked  by  impulses  conveyed  to  certain  cerebro-spinal 
centres  (p.  13).  He  refuses  to  adopt  the  theory  of  cardio- 
arterial  spasm  as  the  indispensable  cause  of  the  pain  (p.  438). 

Professor  Osier,  in  his  erudite  lectures  on  the  subject 
(1897),  after  defining  angina  pectoris,  proceeds  to  say  that 
the  term  is  employed  generically  to  define  paroxysmal 
attacks  of  pain  in  the  chest,  qualifying  the  varieties  by  such 
names  as  true,  false,  hysterical,  and  vasomotor  (p.  8). 

Sir  Douglas  Powell,  in  a  very  admu^able  article, 
classifies  angina  pectoris  under  (1)  a  vasomotor  group,  and 
(2)  angina  pectoris  gravior,  wbich  includes  secondary  and 
primary  cardiac  angina.  Forbes,  Bramwell,  Gibson,  Oliver, 
and  others  recomise  two  classes,  organic  and  functional. 
Huchard  insists  that  there  is  only  one  angina  pectoris,  and 
that  it  is  always  due  to  ischemia  of  the  heart  muscle. 

From  all  this  it  is  quite  clear  that  the  term  is  no  longer 
confined  to  the  severe  and  fatal  malady  described  by 
Heberden.  It  has  been  extended  to  a  great  variety  of 
conditions,  characterised  by  some  sense  of  precordial  dis- 
comfort, or  of  discomfort  referred  directly  to  the  heart,  which 
may  or  may  not  be  accompanied  hy  pain,  and  which  may  or 
may  not  be  associated  with  coarse  anatomical  lesion.  It  was 
to  cover  these  lesser  manifestations  that  such  terms  as 
pseudo-angina,  angina  notha,  false  angina,  and  functional,  as 
distinct  from  organic,  have  been  used  and  applied. 

Angina  is  indeed,  to  use  Osier's  words,  "  a  syndrome  or 
symptom  group,"  the  clinical  pathology  of  wdiich  has  to  be 
determined  in  each  separate  instance.  The  term  angina 
pectoris  has  in  fact  the  same  nosological  significance  as  the 
term  dropsy  formerly  had.  It  is  not  a  disease ;  it  is  a 
symptom  or  a  group  of  symptoms,  and  it  is  no  longer  the 
symptom  but  the  cause  behind  and  determining  it  which  is 
the  problem  presented  to  the  clinical  pathologist  of  to-day. 

Constructive  and  Critical. — In  turning  to  the  con- 
structive side  we  have  to  look  at  certain  vasomotor  pheno- 
mena which  are  to  be  observed  in  the  body ;  and  I  hope  to 
make  it  clear  what  I  regard  to  be  the  relations  of  those 
phenomena  to  the  phenomena  of  angina  pectoris. 

The  presence  of  arterial   spasm  has   been   recognised   by 

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ANGINA  PECTORIS 

many  who  have  written  on  angina  pectoris  since  the  date 
of  Lauder  Brunton's  epoch-making  discovery.  Views  as  to 
the  causation  of  the  spasm  have  heen  various,  and  the 
relation  of  the  spasm  to  the  symptoms  has  also  been 
variously  interpreted. 

An  Arterial  Abdominal  Reflex.— We  have  to  consider 
certain  observations  regarding  an  arterial  reflex  having  its 
origin  in  the  abdomen,  the  importance  of  which  I  think  has 
not  hitherto  been  fully  appreciated.  After  taking  food,  and 
for  at  least  part  of  the  time  during  which  the  active  processes 
of  digestion  are  under  way,  there  is  an  influx  of  blood  to 
the  whole  splanchnic  area,  leading  to  hyperemia,  such  a 
hyperemia  as  considerably  reduces  the  volume  of  blood 
in  parts  outside  this  area.  This  drainage  into  the 
abdominal  vessels  is  balanced  in  the  general  circulation  by 
a  systemic  arterial  contraction.  This  is  evidently  a  reflex 
phenomenon  originating  in  the  splanchnic  system,  passing 
to  the  vasomotor  centre  in  the  medulla,  and  thence  trans- 
mitted to  the  systemic  arteries.  The  existence  of  this  set  of 
phenomena  has  been  carefully  worked  out  by  Dr.  George 
Oliver  in  the  average  healthy  person.  The  arterial 
contraction  is  shown  by  a  definite  diminution  in  the 
diameter  of  the  vessels.  It  is  to  be  regarded  as  a 
physiological  hypertonic  contraction.  The  fact,  then,  with 
which  I  begin  is  the  change  in  tlie  systemic  arteries  during 
active  digestion — whether  it  be  called  narrowing,  contraction, 
or  hypertonus,  signifies  not,  so  long  as  the  word  we  use 
expresses  our  thought.  The  change  will  be  found  to  be  a 
reduction  in  size  and  an  apparent  thickening  of  the  arterial 
wall.  The  degree  of  these  arterial  changes  depends  upon  the 
kind  of  meal  which  has  been  taken.  In  the  big  flesh-eater 
and  the  wine-drinker  the  arterial  contraction  is  associated 
with  a  rise  of  blood-pressure  and  a  true  increase  of  arterial 
tension. 

Putting  extreme  cases  aside,  the  general  statement  will 
be  found  to  be  correct  that  narrowing  of  the  arteries  is 
present,  but  in  many  people,  both  middle-aged  and  old,  I 
do  not  believe  that  there  is  any  constant  rise  of  blood- 
pressure  along  with  it.  The  point  is  not  a  purely  academic 
one,   for  the   small   and   constricted    vessel,  with    its    slight 

136 


ANGINA  PECTORIS 

systolic  expansion,  is  very  commonly  regarded  as  an  indication 
of  heart  debility,  and  treated  as  such.  In  other  cases  the 
mistaking  of  hypertonus  for  a  rise  of  lilood-pressure  may  be 
of  no  practical  consequence,  for  the  treatment  applicable  to 
the  one  is  suitable  for  the  other. 

The  point  here  insisted  on  is  the  existence  of  this 
arrangement  for  adapting  the  circulation  to  the  normal 
processes  of  ingestion  and  digestion  of  food.  It  is  a  normal 
reflex  process.  It  is  a  systemic  vessel  constriction  originating 
in  a  normal  stimulus  in  the  abdomen,  and  brought  about 
through  the  anatomical  connections  in  the  nervous  system. 
It  is  not,  therefore,  a  "  neurosis  " ;  nor  is  the  exaggeration  of 
this  reflex,  prompted  by  a  large  meal  of  stimulating  foods,  a 
neurosis.  It  is  necessary  to  lay  emphasis  on  this  distinction. 
This  reflex,  like  all  normal  reflexes,  is  a  beneficent  arrange- 
ment, and  could  be  easily  shown  to  be  one  of  the  means  of 
protecting  the  body  from  injury.  It  varies  in  delicacy  in 
different  persons  ;  it  exists  in  all. 

Exaggeration  of  Normal  Abdominal  Reflex. — Grantiug  the 
existence  of  this  normal  reflex,  it  will  not  be  questioned  that 
high  feeding  and  alcoholic  liquors  accentuate  it ;  and  that 
under  such  circumstances  there  is  marked  raising  of  arterial 
tension  in  addition  to  arterial  contraction. 

It  must,  however,  be  here  recognised  that  in  the  latter 
conditions  there  are  two  elements  present — one,  the  vascular 
reflex  ;  and  second,  the  passage  into  the  circulation  of 
substances  produced  in  the  processes  of  digestion,  and  of 
substances  derived  from  the  alcoholic  liquors  drunk.  It  is 
not  possible  at  present  to  give  these  two  factors  their  precise 
place  in  bringing  about  tlie  accentuation  of  vessel  constriction 
and  of  stimulating  the  increased  tension.  The  existence  of 
the  reflex  is  granted,  and  there  is  really  little  room  for  doubt 
that  certain  substances  present  in  the  l)lood  directly  stimulate 
vessel  contraction.  Contraction  so  induced  is  not  a  neurosis ; 
it  may,  indeed,  be  induced  when  the'  connection  with  nerve 
centres  is  destroyed. 

Action  of  Reflex  on  Sclerosed  Arteries. — This  recurring 
arterial  contraction,  especially  if  associated  with  increased 
arterial  tension,  is,  as  I  pointed  out  some  time  ago,  the 
efficient  cause,  and  the  usual  cause,  of  arterio-sclerosis  in  the 

137 


ANGINA  PECTORIS 

sense  in  which  this  term  ought  to  be  used.  At  the  same 
time  I  dwelt  upon  the  importance  of  recognising  that 
sclerosed  vessels  are  not,  because  of  the  change  in  their 
walls,  incapable  of  contraction,  but  that,  on  the  contrary,  they 
are  prone  to  become  hypertonic  from  causes  which  are 
commonly  regarded  as  trifling.  Professor  Pal,  as  seen  in 
his  recently  published  work,  Gefdsshrisen,  has  also  observed 
that  sclerosed  vessels  are  particularly  sensitive,  and  specially 
liable  to  hypertonic  contraction. 

Let  us  bear  in  mind  then — First,  the  existence  of  tlxis 
systemic  arterial  reflex  having  its  origin  in  the  digestive 
organs  or  processes.  Secondly,  the  influence  of  the  character 
of  the  material  introduced  into  the  digestive  system  in 
accentuating  the  reflex.  Tlbirclly,  the  effect  of  the  reflex  in 
producing  arterio-sclerosis.  Fourthly,  that  sclerosed  vessels 
are  particularly  liable  to  hypertonic  contraction. 

Relation  of  Reflex  to  Angina  Pectoris. — The  relation 
between  the  phenomena  just  dealt  witli  and  angina  pectoris  is 
not  at  first  sight  apparent  :  and,  in  order  to  demonstrate  the 
close  connection  between  the  two,  I  must  now  as  briefly  as 
possible  refer  to  several  illustrative  cases  which  I  have 
recently  observed. 

Case  56. — Angina 'pectoris  gravior,  sliowing  extreme  sensi- 
tiveness- of  arterio-carcliac  reflex  and  its  production  hy  taking 
nourishment.- — The  patient  was  a  professional  man,  aged  67, 
whom  I  saw  for  the  first  time  on  6th  September  1904.  He 
had  suffered  for  years  from  definite  and  characteristic  attacks 
of  angina  pectoris.  Lately  he  had  been  much  worse,  and  had 
been  confined  to  Ijed  for  weeks.  When  I  first  saw  him  he 
was  having  many  attacks  daily,  and  circumstances  of  the 
most  ordinary  kind  evidently  brought  them  on — such 
circumstances  as  the  taking  of  nourishment,  the  presence 
of  flatulence,  slight  excitement,  and  even  the  changing  of 
his  position  in  bed.  The  severity  of  the  attacks  varied 
within  considerable  limits  ;  the  more  severe,  and  therefore 
the  more  typical,  attacks  began  with  pain  in  the  left  elbow, 
which  soon  extended  upwards  to  the  shoulder  and  then 
downwards  over  the  precordia.  During  an  attack  the  hands 
became  cold  and  painful.      The  medical  attendant,  who  was 

138 


ANGINA  PECTORIS 

watching  the  patient  with  the  greatest  assiduity,  informed  me 
that  the  pulse  always  indicated  the  advent  of  an  attack  ;  the 
radial  artery  became  more  definite,  firmer,  and  smaller  ;  the 
pulse  rate  increased  ;  while  the  wave  became  small,  and  might 
almost  disappear.  In  some  of  the  worst  attacks  the  patient 
had  become  unconscious  and  was  thought  to  be  dving.  The 
treatment  followed  was  the  administration  of  nitrite  of  amyl 
and  nitroglycerine  for  the  more  pronounced  of  the  attacks, 
and  the  relief  afforded  by  them  had  always  been  prompt. 
Under  the  influence  of  one  or  other  the  pulse  wave  became 
larger,  the  vessel  wall  softer,  the  hands  became  warm,  and  the 
pain  passed  off.  The  patient  took  a  remarkably  calm  and 
intelligent  interest  in  his  attacks,  and  the  foregoing  is  gleaned 
from  his  own  and  the  medical  attendant's  description.  The 
diet  for  some  time  had  consisted  almost  exclusively  of 
raw  eggs  and  weak  Ijroth,  while  sedatives  of  various  kinds 
had  been  employed  medicinally.  The  patient  had  always 
been  a  large  flesh-eater.  There  was  no  albumen  or  sugar  in 
the  urine.  The  medical  attendant  had  been  impressed  by 
the  fact  that  the  patient  more  recently  almost  always  had 
a  seizure  after  being  given  nourishment,  even  when  that 
consisted  of  some  raw  egg.  I  had  the  opportunity  of 
confirming  the  observations  on  the  change  in  the  pulse 
during  a  paroxysm  soon  after  my  arrival  at  tlie  patient's 
bedside.  During  the  time  I  spent  talking  quietly  to  him  the 
pulse  was  small,  soft,  and  feeble.  I  examined  the  heart 
without  causing  any  discomfort.  The  sounds  were  so  faint 
that  they  were  occasionally  inaudible,  although  the  chest 
wall  was  thin.  I  next  proceeded  to  examine  the  abdomen, 
and  had  my  hand  placed  quite  lightly  on  the  epigastrium 
when  the  patient  told  us  that  an  attack  was  coming  on. 
I  at  once  removed  my  hand.  He  took  his  attack  with 
remarkable  composure,  and  it  was  evidently  not  accompanied 
Ijy  the  distressing  sensations  which  so  frequently  accompany 
anginal  seizures.  Pain  began  in  the  left  elbow,  which,  as  has 
already  been  noted,  was  always  the  premonitory  symptom  of 
the  more  severe  seizures,  and  extended  to  the  shoulder  and 
then  to  the  precordia.  The  face  became  pale.  The  radial 
artery  became  quite  abruptly  hypertonic — that  is,  it  became 
firmer  and  smaller,  the  rate  rose  to  100   and  110,  and  the 

139 


ANGINA  PECTORIS 

tension  was  sensibly  raised.  He  was  at  once  given  a  tabloid 
of  nitroglycerine,  and  in  a  very  short  time  the  artery  relaxed 
and  the  pulse  became  large,  strong,  and  rather  thumping,  the 
pallor  of  the  face  was  exchanged  for  a  ruddy  tint,  and  the 
pain  ceased.  The  thumping  soon  passed  off,  and  the  pulse 
resumed  the  small,  feeble  character  it  had  presented  at  the 
outset. 

Comments. — There  could,  of  course,  be  no  doubt  that  the 
patient  was  the  victim  of  a  severe  form  of  angina  pectoris, 
and  that  the  attacks  were  accompanied  by  marked  arterial 
constriction.  It  was  fortunately  easy  to  arrest  the  seizures. 
They  had,  however,  persisted  for  weeks  without  any  lessening 
in  their  frequency  or  in  their  severity.  The  question  which 
awaited  solution  was.  Could  anything  be  done  to  lessen  the 
tendency  to  the  attacks  ?  Palliation  was  easily  achieved ; 
but  could  any  measures  be  adopted  which  might  be  more 
curative  ?  The  point  in  the  history  which  was  most  un- 
common was  the  fact  that  the  taking  of  nourishment  was 
almost  always  followed  by  an  attack,  although  the  amount 
taken  was  small  and  could  hardly  be  further  reduced.  Acting, 
however,  on  this  indication,  it  was  decided  to  materially  alter 
the  diet,  the  nature  of  which  has  been  already  stated.  The 
dietary  now  advised  was  to  consist  of  peptonised  milk, 
peptonised  oatmeal  gruel,  etc.,  and  one  raw  egg  well  beaten 
up,  daily.  The  patient  was  moreover  given  small  doses  of 
arsenic,  tincture  of  strophanthus,  and  spirits  of  nitrous  ether. 
This  line  of  treatment  was  persisted  in,  and  when  I  saw  the 
patient  a  fortnight  later  the  report  of  his  condition  showed 
considerable  and  satisfactory  improvement,  the  attacks  had 
greatly  diminished  in  number  and  severity,  and  the  taking 
of  nourishment  was  only  occasionally  followed  by  an  attack ; 
the  pulse  was  stronger.  The  tongue,  however,  had  become 
coated,  and  small  doses  of  rhubarb  and  soda  were  advised. 

A  week  later  the  report  was  that  the  attacks  had  still 
further  lessened  in  severity  and  frequency,  and  that  when 
an  attack  was  threatened  it  could  be  averted  by  a  dose  of 
aromatic  spirit  of  ammonia  or  even  by  a  dose  of  rhubarb 
and  soda  mixture.  When  pain  in  the  elbow  came  on,  it 
was  accepted  as  an  indication  that  the  threatened  attack 
would   be    somewhat    severe,   and    the    patient  was   at  once 

140 


ANGINA  PECTORIS 

given  a  small  dose  of  nitrite  of  amyl.  The  sensations 
which  now  more  ordinarily  preceded  an  attack  were  a 
sense  of  discomfort  and  distention  in  the  stomach,  and 
attacks  were  often  associated  with  definite  flatulent 
distension,  the  escape  of  gas  being  followed  hj  relief. 
The  medical  attendant  noted  that  when  the  abdominal 
discomfort  supervened  the  pulse  rate  increased,  and  there 
was  distinct  hypertonus ;  as  the  attack  passed  the  vessel 
wall  relaxed  and  the  rate  returned  to  normal.  Within  the 
next  two  months  the  patient's  condition  varied  a  good  deal, 
iDut  it  was  noted  that  any  gastro-intestinal  or  digestive 
upset  at  once  threatened  to  induce  an  increased  number  of 
attacks.  The  management  of  the  diet  and  of  the  digestive 
system  required  much  tact  and  judgment,  and  was  admirably 
conducted  by  the  doctor  in  charge.  In  some  weeks  the  patient 
had  improved  so  much  that  he  was  able  to  be  out  of  bed  and 
to  move  about  the  house  for  the  greater  part  of  each  day, 
and  to  interest  himself  in  outside  affairs.  His  clinical  history 
for  the  succeeding  months  was  chequered,  for  as  his  condition 
improved,  it  became  impossible  to  continuously  diet  him  as 
was  desirable ;  still,  at  the  end  of  June  1905  he  had  not 
had  a  seizure  for  six  weeks,  and  was  in  fact  freer  of  attacks 
than  he  had  been  for  years. 

Soon  after  this,  however,  albuminuria  made  its  appear- 
ance with  anasarca.  The  anasarca  was  got  rid  of,  but  the 
albuminuria  persisted ;  Cheyne-Stokes  breathing  developed 
and  became  extreme.  The  patient  finally  developed  gangrene 
of  his  entire  right  lower  limb,  of  which  he  died  in  the  end 
of  October  1905,  a  proof  that  his  arterial  system  was  more 
degenerate  than  the  radials  indicated.  I  submit  the  case  as 
illustrating  an  extreme  exaggeration  of  the  normal  reflex 
which  has  been  described.  The  angina  in  this  patient  was 
associated  with  a  weak  and  somewhat  enlarged  heart.  The 
hypertonic  spasm  of  systemic  arterioles,  resulting  from 
gastro-intestinal  stimulus,  proved  so  severe  a  strain  on  the 
weakened  heart  as  frequently  to  lead  to  a  syncope,  during 
the  anginal  paroxysm,  which  was  only  short  of  being  fatal. 
If  we  had  had  the  opportunity  of  seeing  the  heart,  it  is 
probable  that  atheromatous  or  ossified  coronary  arteries 
would  have  explained  its  debility.      The  instructive  feature 

141 


ANGINA  PECTORIS 

was  the  extraordinary  sensitiveness  of  the  peripheral  organs 
from  which  the  reflex  started,  and  the  success  in  allaying 
that  sensitiveness  by  changing  the  kind  of  nourishment  given, 
and  its  partial  predigestion.  The  remedial  effect  was  so 
pronounced  that  it  gave  me  the  impression  that  in  this 
patient  the  normal  reflex  had  been  irritated  beyond  control 
by  the  free  use  of  the  more  pure  proteid  foods,  until  it 
responded  to  the  most  trifling  local  irritation.  That  the 
anginous  symptoms  were  always  determined  by  the  vascular 
hypertonic  contraction  was  undoubted,  and,  so  long  as  the 
latter  could  be  restrained,  there  was  no  angina,  and,  as  has 
been  indicated,  the  key  of  the  position  was  in  the  alimentary 
system. 

Case  57. — Condition  allied  to  angina,  sJiotoing  the  stimu- 
lation of  the  arterio-eardiac  reflex  'by  digestive  disturhance. — 
This  case  might  be  classed  as  angina  sine  dolore,  but  I  use  it 
as  an  example  of  conditions  allied  to  angina  pectoris,  in  which 
hypersensitiveness  of  the  abdominal  reflex  gave  rise  to  pheno- 
mena of  considerable  interest  and  importance. 

The  patient,  aged  68,  was  a  member  of  one  of  the  learned 
professions,  and  had  spent  many  years  in  the  tropics.  I 
saw  him  in  November  1904,  during  convalescence  from  an 
influenzal  broncho-pneumonia,  and  was  informed  that  on  the 
afternoon  of  the  previous  day,  between  four  and  flve  o'clock, 
he  had  had  a  "  fainting  attack,"  in  which  his  face  became  pale, 
he  broke  out  into  a  cold  perspiration,  and  the  pulse  was 
imperceptible.  The  nurse  had  been  greatly  alarmed,  as  she 
thouQ-ht  the  patient  was  dvins;.  He  soon,  however,  rallied 
from  this,  and  I  saw  him  in  the  afternoon  of  the  following 
day.  It  is  unnecessary  to  enter  into  the  details  of  this  case 
at  this  stage,  beyond  saying  that  when  the  medical  attendant 
and  I  inquired  fully  into  his  dietary,  it  was  found  to  be  very 
faulty,  and  he  was  forthwith  put  upon  a  comparatively  austere 
regimen. 

He  had  no  similar  attacks  during  the  following  days, 
but  he  often  spoke  of  an  attack  as  impending,  and  he 
apparently  expected  an  attack  about  four  o'clock  in  the 
afternoon.  It  was  thought  by  his  family  and  the  nurse  that 
this    was     pure     nervousness,    and     an     expression     of     the 

142 


ANGINA  PECTORIS 

pessimistic  view  he  tended,  to  tal^e  of  his  condition.  Five 
days  later  I  again  saw  the  patient,  and  obtained  from  the 
nurse  the  statements  on  wliich  the  preceding  account  is 
based.  I  w^as  waiting  by  the  patient's  bedside  for  his 
medical  attendant  to  arrive,  and  thought  the  patient,  who 
was  sitting  propped  up  in  bed,  looking  well,  for  his  colour 
was  good.  His  pulse  was  80,  soft,  small,  and  feeble.  The 
respiration,  however,  showed  a  long  deep  breath  often  with 
a  little  sigh,  followed  by  several  quiet  inspirations ;  it  was 
distinctly  "  cerebral "  in  type,  and  it  made  me  somewhat 
anxious.  I  asked  the  nurse  to  give  him  half  an  ounce  of 
whisky  in  water,  although  he  had  had  a  couple  of  drachms 
shortly  before,  as  I  wanted  to  see  the  effect  it  would  have 
upon  the  pulse  and  respiration.  The  effect  was  unexpectedly 
striking,  and  even  alarming.  In  a  few  seconds  the  pulse 
altered  greatly  in  character :  the  artery  very  plainly 
tightened  up,  becoming  smaller  and  harder,  and  the  rate 
varied  within  very  wide  limits.  It  was  frequently  88  per 
minute,  then  it  would  run  up  to  over  100,  and  again  some- 
times fall  even  to  40.  Along  with  this  sudden  irregularity 
in  the  pulse  rate  there  were  equally  pronounced  respiratory 
and  cerebral  phenomena.  Lying  with  his  eyes  shut,  the 
patient  seemed  to  fall  asleep,  and  the  breathing  was  so 
quiet  and  shallow  that  only  on  close  attention  could  it  be 
seen  that  he  was  breathing  at  all.  Then  he  wakened  up 
with  a  start  and  a  groan,  followed  by  some  deep  breaths. 
This  series  of  phenomena  went  on  with  perfect  regularity  as 
long  as  he  was  not  spoken  to,  each  part  of  the  cycle  only 
lasting  some  seconds.  When  asked  on  awakening  what  was 
the  matter,  lie  explained  that  he  had  become  unconscious, 
and  had  been  dreaming  that  he  was  falling  down  a  precipice, 
or  passing  through  some  equally  unpleasant  experience,  often 
in  company  with  some  old  friend  long  dead.  He  spoke  of 
these  attacks  as  "  delirium,"  and  insisted  that  the  present 
was  only  an  exaggeration  of  what  he  had  experienced  every 
afternoon,  and  to  which  reference  has  already  been  made. 
He  could  be  kept  aw^ake  by  speaking  to  him,  and  he  pre- 
ferred Ijeing  spoken  to,  because,  as  he  said,  it  helped  him  to 
fight  against  the  attacks.  When  he  woke  up  from  the 
nightmare  his  words  were    sometimes   incoherent   and  unin- 

143 


ANGINA  PECTORIS 

telligible  for  a  few  seconds,  but  he  rapidly  regained  complete 
self-possession. 

This  alarming  and  curious  condition  lasted  about  an 
hour.  It  had  come  on  about  three  hours  after  lunch,  which 
had  consisted  of  a  chop,  spinach,  and  one  potato.  Some  time 
after  that  he  had  had  milk  and  hot  water  and  two  drachms 
of  whisky  in  lieu  of  afternoon  tea.  When  the  patient's 
condition  was  as  has  been  described,  I  asked  the  nurse  to 
make  some  tea,  and  he  was  given  two-thirds  of  a  moderate- 
sized  cupful  of  this.  The  attack  had  completely  passed  off 
by  the  time  the  doctor  arrived ;  the  pulse  had  returned  to 
the  condition  it  was  in  before  the  attack,  the  breathing  was 
regular,  and  he  was  quite  calm  and  self-possessed.  When 
the  next  meal  came  he  was  quite  able  to  feed  himself.  I 
had  no  doubt  the  patient's  view  was  correct  that  the 
symptoms  shown  this  particular  afternoon  were  only  an 
exaggeration  of  the  afternoon  symptoms  which  he  had 
spoken  of,  but  which  no  one  with  more  understanding  than 
a  nurse  had  witnessed.  The  doctor  had  called  at  various 
hours  for  the  purpose  of  observing  the  attacks,  but  the 
stimulus  of  his  visit  appeared  to  be  sufficient  to  postpone 
them. 

Comments. — The  phenomena  in  this  case  were  very 
striking,  and  the  symptoms  could  only  be  regarded  as 
indicating  an  anxious  condition  of  matters.  The  fact  that 
they  threatened  chiefly  in  the  afternoon,  and  had  so  far 
lasted  only  for  a  comparatively  short  time  each  day,  was 
reassuring  ;  while  the  time  of  their  occurrence  suggested  a 
connection  between  the  symptoms  and  the  stage  of  the 
digestion  of  the  midday  meal,  which  was  the  principal 
meal  of  the  day.  Suspicion  was  all  the  more  strongly 
directed  to  this  view  by  the  fact,  of  which  I  had  no  doubt, 
that  the  attack  I  witnessed  was  precipitated  or  intensified 
by  the  half-ounce  of  whisky  given  at  my  suggestion.  The 
immediateness  of  the  effect  was  startling :  it  gave  the  im- 
pression of  being  produced  the  moment  the  draught  reached 
the  stomach.  It  was  indeed  impossible  to  escape  from  the 
conviction  that  the  phenomena  pointed  to  the  production  b}^ 
the  alcohol  of  a  peripheral  gastric  irritation  or  stimulation, 
which    precipitated    or    intensified    a    condition    which    was 

144 


ANGINA  PECTORIS 

already  threatening.  On  this  assumption  the  local  irritation 
must  have  been  followed  by  a  very  prompt  reflex  effect. 
The  impulse  communicated  by  the  sensory  nerves  of  the 
stomach  to  the  vasomotor  centre  must  have  stimulated  that 
centre  so  as  to  increase  its  vaso-constrictor  action,  the  result 
being  the  hypertonic  contraction  of  the  radial  artery  which 
was  so  markedly  present.  This  stimulation  of  the  vaso- 
motor centre  must  have  also  told  in  some  way  upon  the 
cerebral  blood  supply,  judging  from  the  cerebral  manifesta- 
tions which  were  present.  That  even  the  motor  area  of 
the  brain  was  involved  was  shown  by  the  occurrence  of 
muscular  twitching  and  starting  of  the  limbs,  especially  on 
the  right  side,  when  the  other  cerebral  manifestations  were 
at  their  maximum.  The  respiratory  centre,  as  shown  by 
the  great  respiratory  irregularity,  shared  in  the  perturbation. 
This  association,  however,  is  of  common  occurrence.  That 
the  attack  should  have  passed  off  as  it  did,  without  any 
therapeutic  measures  being  taken  beyond  the  administration 
of  a  few  ounces  of  tea  infusion,  only  strengthened  the  view 
that  it  had  been  determined  by  peripheral  conditions  of  a 
temporary  kind ;  that,  indeed,  the  true  cause  of  the  trouble 
lay  in  an  error  in  the  digestive  process  at  this  particular 
period  after  the  midday  meal. 

The  diet  was  altered  in  some  of  its  details,  and  for  an 
afternoon  or  two  the  patient  was  given  a  dose  of  one  of  the 
commonly  used  vaso-dilators  as  soon  as  the  symptoms 
threatened  to  come  on.  He  had  no  more  attacks ;  his 
recovery  was  complete,  and  he  returned  to  his  duties  in  the 
East.  Nearly  three  years  later  there  had  been  no  recurrence 
of  the  symptoms. 

Case  58. — Anginous  paroxysms  first  ap'pearing  on 
2iliysical  effort:  influence  of  emotion  and  of  diet. —  This 
patient  was  a  public  -  servant,  whom  I  saw  in  July  1905. 
He  had  suffered  for  some  time  from  attacks  of  typical 
angina  pectoris,  commencing  with  pain  referred  to  the 
heart.  This  symptom  first  appeared  when  he  was  hunting, 
and  so  constantly  reappeared  when  he  attempted  to  follow 
the  hounds  that  he  had  to  stop  doing  so.  He  had  had  one 
or  two  attacks  of  great  severity  during  the  niglit,  in  at  least 
K  "  145 


ANGINA  PECTORIS 

one  of  which  it  was  thought  he  was  to  die.      He  had  been 
treated    with     considerable     success     by    an     eminent    Irish 
physician.      He  carried    about    tabloids    of    trinitrin    in    his 
waistcoat  pocket,  and  had  been  taking  potassium  iodide  for 
some  time.      His  condition  had  become  practically  stationary : 
hunting  was  out   of    the  question ;    he  could  only  walk  on 
level    ground ;    the    slightest    hill,    or    the    slightest    hurry, 
produced    a    breast    pang,   which    arrested    further    activity. 
When  I  first  saw  him  he  was  having  a  slight  attack  almost 
nightly,  soon  after   midnight,  and   at    that   time  he'  usually 
took  a  tabloid  of  trinitrin.      He  claimed  to  be  a  small  eater, 
and  his  daily  wine  consumption  did  not  exceed  two  or  three 
glasses.      His  dietetic  habits  had  not  been  seriously  inquired 
into,  and  had  not  been  altered.      He  had  been  told  that  the 
artery  of  his  heart  was  rigid,  and  he  and  his  family  were 
dwelling  under  the  shadow  of  the  fear  of  sudden  death  at 
any  moment.      On  examining  him   I   found   that   the  heart 
was  slightly  enlarged,  the    dulness    reaching  to    the   nipple 
line,  but  the  sounds  were  clear  and  pure  at  apex  and  base. 
The  pulse  was  regular,  of  good  strength,  and  gave  no  indica- 
tion   of    an    enfeebled    myocardium.      The    vessel    wall   was 
much  thickened  for   a  man  of  his  age,  and  in  view  of  the 
arduous  life  he  had  led  at  home  and  abroad ;  there  was  no 
albumen  or  sugar  in  the  urine,  but  it  tended  to  be  scanty 
and  high-coloured.      The  bowels  were  acting,  but  not  freely, 
and  his  conjunctivte  indicated  "  sluggish  liver."     The  question 
here,  as  in  Case  I.,  was  whether  anything  could  be  done  to 
carry  improvement  beyond  the  point  it  had  reached.      I  was 
again  fortunate  in  witnessing  a  slight  attack  in  this  patient. 
When  I  was    examining  into    the    state    of    his    heart  and 
vessels,  which   under   the    circumstances   I   was   doing   with 
great  care,  and  not    hurriedly,  he    became  a  little  agitated, 
and  informed  me  that  he  was  having  a  slight  attack,  with 
the  usual  feeling  in  his  heart.      On  putting  my  finger  on  the 
radial  pulse,  it  had  become  markedly  hypertonic.      In  a  very 
short  time  the  hypertonic  spasm  relaxed,  and  the  heart  sen- 
sation vanished. 

Here  was  another  instance  of  the  pain  and  anxiety  of 
angina,  assuredly  due  to  arterial  spasm.  There  seemed  to 
me,  further,  no  doubt  that  the  measure    of    emotional    dis- 

146 


ANGINA  PECTORIS 

turbance  aroused  by  the  medical  examination  had  induced 
the  attack.  There  was,  therefore,  no  doubt  as  to  the 
existence  of  marked  vasomotor  sensitiveness.  As  the  patient 
was  ah^eady  taking  potassium  iodide  more  or  less  regularly, 
and  trinitrin  when  threatened  with  a  paroxysm,  I  felt  that 
not  much  benefit  could  be  expected  from  further  medicinal 
measures.  Guided  again,  therefore,  by  the  theory  that  this 
vasomotor  sensitiveness  owed  its  origin  to  the  circumstances 
and  conditions  of  the  alimentary  system,  I  strongly  ad\ased 
that  all  wine  should  be  stopped,  and  that  other  changes  be 
made  in  the  diet.  The  progress  of  the  case  need  not  be 
enlarged  upon ;  it  is  sufficient  to  say  that  the  patient  made 
marked  improvement  in  every  respect.  Two  years  later  this 
patient  was  reported  as  in  good  health. 

Case  5  9. — Angina  vnth  gastric  disorder  :  attack  caused 
ly  'palpation  of  epigastrium. — This  was  a  female  patient  in 
the  Eoyal  Infirmary,  who  complained  of  attacks  of  pain  in 
the  chest,  over  the  precordia,  with  shortness  of  breath  and 
of  indigestion  and  pain  in  the  epigastrium.  The  heart  was 
weak  and  somewhat  dilated.  I  mention  this  case  on  account 
of  an  experience  I  had  in  connection  with  it  somewhat  re- 
sembling an  incident  noted  in  Case  I.  On  examining  the 
patient's  abdomen  I  found  that  there  was  siu'face  hypertesthesia- 
in  the  epigastrimn,  as  is  common  in  some  forms  of  gastric 
disturbance :  and  as  I  was  gently  palpating  the  region,  I 
noticed  the  patient's  face  become  pale  and  expressive  of 
anxiety  and  discomfort.  I  at  once  put  my  finger  on  the 
pulse,  and  asked  her  what  was  the  matter ;  she  replied 
that  the  pain  in  her  chest  had  come  on.  The  radial  artery 
had  become  markedly  contracted  and  hardened.  As  the 
hypertonic  spasm  of  the  artery  relaxed  the  heart  discom- 
fort passed  off. 

Clinical  Pathology.  —  By  gathering  up  the  separate 
points,  we  are  able  to  explain  the  whole  clinical  pathology 
of  angina  pectoris.  In  the  first  place,  there  may  or  may  not 
be  a  morbid  anatomy.  AYhen  present,  it  varies  so  widely  in 
different  instances  that,  from  the  earliest  times  to  the  present, 
many  physicians  have  refused  to  accept  any  anatomical  change 
as  sufficient  to  explain  the  phenomena.      Whenever  this  is 

147 


ANGINA  PECTORIS 

the  state  of  knowledge,  it  will  be  found  that  men  turn  to  that 
scapegoat  of  all  that  is  unknown — the  nervous  system. 

In  attempting  to  interpret  the  phenomena  of  angina 
pectoris,  I  shall  begin  with  an  illustration  of  the  simplest 
form  of  angina.  Tobacco  poisoning,  from  smoking,  is 
commonly  recognised  as  the  cause  of  a  form  of  angina 
pectoris — a  toxic  angina.  It  so  happens  that  I  can  give 
myself  tobacco  angina  by  smoking  strong  tobacco.  The 
symptom  which  arouses  me  to  the  fact  that  I  must  put 
my  pipe  aside  is  a  sense  of  constriction  at  the  heart,  a 
feeling  as  if  it  were  grasped ;  it  is  not  a  very  unpleasant 
sensation,  but  it  gives  one  the  impression  that  it  only 
required  to  be  much  intensified  to  make  the  dolor  pectoris 
to  be  avoided,  whatever  self-denial  it  required.  The  heart 
discomfort  is  accompanied  by  a  hypertonic  contraction  of 
the  radial  arteries.  Discomfort  and  hypertonus  disappear 
together.  If  I  am  told  this  is  a  neurosis,  all  I  can  reply 
is,  if  it  is,  opium  poisoning,  or  tetanus,  is  also  a  neurosis ;  and 
that  I  do  not  look  at  morbid  processes  from  that  standpoint. 

Whatever  the  degree  of  intensity  the  heart-pang  may 
reach,  it  is,  I  believe,  always  the  result  of  a  sudden 
embarrassment  of  the  myocardium,  and  usually  and  chiefly 
that  of  the  left  ventricle.  This  sudden  heart  embarrassment, 
varying  widely  in  degree  and  intensity,  is  the  one  fact 
common  to  all  the  divisions  or  subdivisions  under  which 
all  cases  have  been  classed.  The  angor  animi,  which  also 
varies  in  degree,  is,  I  think,  common  to  all  sudden  heart 
embarrassments,  which  fall  short  of  being  so  immediately 
fatal  that  there  is  no  time  for  the  development  of  such 
sensations. 

Professor  Clifford  Allbutt  attributes  the  pain  to  an 
aortitis  or  a  periaortitis.  When  either  of  these  is  present,  the 
raising  of  aortic  pressure  following  upon  arterial  contraction 
may  well  cause  a  pain  comparable  to  pain  caused  as  I  have 
just  indicated. 

The  heart  embarrassment  is,  as  Mackenzie  has  quite 
recently  pointed  out,  an  "  impairment  of  the  function  of 
contractility."  This  is  the  modern  expression  of  what  Parry 
meant  by  "  syncope."  It  is  to  this  condition,  associated  with 
pain,  that  Eosenbach  confines  the  term  "  stenocardia." 

148 


ANGINA  PECTORIS 

The  impaired  contractility  is  due  either,  in  the  first 
place,  to  the  sudden  strain  put  upon  a  feeble  myocardium 
by  general  arterial  contraction,  or  by  a  call  for  increased 
work ;  or,  in  the  second  place,  to  a  myocardium  feeble,  not 
from  anatomical  changes  in  it,  but  temporarily  so,  from 
deficient  blood  supply,  the  result  of  the  participation  of  the 
coronary  arteries  in  a  general  arterial  spasm. 

The  cause  of  the  sudden  heart  embarrassment  in  the  vast 
majority  of  cases  is  the  arterial  hypertonic  contraction,  or 
spasm  contraction,  we  have  been  considering  ;  the  latter  term 
indicating  the  more  sudden  and  severe  degrees  of  contraction. 
Even  toxic  conditions  only  give  rise  to  angina  when  the  factors 
indicated  are  present. 

By  means  of  the  cases  reported  I  have  endeavoured  to 
illustrate  the  remarkable  relations  which  exist  between 
the  digestive  system,  or  the  materials  introduced  into  it, 
and  the  general  arterial  system.  I  have  also  shown  that 
conditions  having  their  origin  in  the  abdomen  can  induce 
a  hypersensitiveness  of  a  normal  vasomotor  reflex,  which 
becomes  apparent  as  arterial  spasm,  whenever  the  exciting 
conditions  are  sufficiently  pronounced ;  and  that  when  those 
conditions  are  altered  the  arterial  spasm  disappears. 

As  I  have  already  indicated,  the  arterial  spasm  may  be 
determined  by  direct  irritation  of  the  stomach.  In  two  of  the 
preceding  cases  the  spasm  and  its  accompanying  paroxysm  of 
angina  were  caused  by  palpation  of  the  epigastrium.  This 
illustrates  the  well-known  nerve  connection  between  surface 
and  viscera — gastric  disorders  frequently  causing  surface 
hyperesthesia,  while  in  these  two  cases  the  surface  stimulus 
produced  the  same  effect  as  if  a  stimulus  had  been  applied 
directly  to  that  viscus. 

The  stimulus  is  also  provided  by  the  substances  taken 
into  or  absorbed  from  the  alimentary  tract.  These  substances 
exercise  a  supreme  influence  in  producing  and  in  maintaining 
the  hypersensitiveness  of  the  vasomotor  reflex,  and  therefore 
of  the  vasomotor  centre. 

This  hypersensitiveness  of  the  vasomotor  centre  explains 
what  has  long  been  recognised — that  paroxysms  of  angina 
have  as  their  main  determining  cause  physical  effort,  mental 
emotion,  or  digestive  disturbance. 

149 


ANGINA  PECTORIS 

The  Unifying  Principle. — By  the  application  of  the 
facts  I  have  brought  under  review  the  group  of  symptoms 
known  as  angina  pectoris  can  be  satisfactorily  explained,  no 
matter  how  diverse  the  conditions  may  be  in  which  it  occurs. 
It  explains  the  occurrence  of  the  symptoms  without  anatomical 
change,  while  at  the  same  time  it  shows  the  importance  of  the 
presence  of  anatomical  changes  in  the  coronary  arteries,  or  in 
the  myocardium.  In  this  connection  it  must  always  be  borne 
in  mind  that  even  calcareous  coronary  arteries  are  not 
calcareous  to  their  finer  subdivisions,  so  that  in  this  condition, 
as  well  as  in  the  varying  degrees  of  arterio-sclerosis,  the 
power  of  spasm  contraction  is  not  lost — may  indeed  be 
intensified.  It  gives  to  the  nervous  system  its  due  place 
in  the  production  of  the  phenomena. 

To  illustrate  the  production  of  a  paroxysm  by  mental 
emotion  or  physical  effort,  let  me  refer  to  Case  58,  in  which 
slight  emotional  disturbance  or  slight  exertion  had  the  effect 
of  inducing  a  paroxysm.  The  connection  between  the 
emotional  centres  and  the  vasomotor  centre  is  a  normal 
one,  and  constantly  active.  In  this  case  a  normal  emotional 
impulse  acted  upon  the  hypersensitive  vasomotor  centre, 
resulting  in  the  arterio-cardiac  phenomena  of  angina.  This 
was  no  abnormal  excitation  of  any  emotional  centre.  It  was 
a  normal  excitation  passing  on  to  an  abnormally  sensitive 
vasomotor  centre.  The  vasomotor  centre  in  this  same  patient 
was  equally  influenced  by  slight  physical  effort ;  it  was  not 
the  voluntary  muscle  centres,  nor  the  nerve  endings  in  the 
muscles,  which  were  unduly  sensitive,  but  the  vasomotor 
centre  to  the  normal  influences  resulting  from  voluntary 
muscular  eflbrt. 

By  the  cases  reported  I  have  also  shown  that  this 
hypersensitiveness  of  the  vasomotor  centre,  even  in  grave 
angina  pectoris,  can  be  reduced,  controlled,  or  even  removed 
by  dietetic  measures,  with  the  result  that  the  anginous 
seizures  are  removed  or  greatly  modified.  In  cases  where 
the  arterial  spasm  is  associated  with  great  anatomical  change, 
either  in  the  myocardium  or  in  the  coronary  vessels,  absolute 
cure  can  hardly  be  looked  for  ;  but  in  all  cases  the  symptoms 
of  angina  pectoris  may  be  much  ameliorated  by  accepting,  as 
a  working   hypothesis,  the   propositions  I  have  ventured  to 

ISO 


ANGINA  PECTORIS 

submit,  and  conducting  the  treatment  in  accordance  with 
what  they  indicate. 

There  was  need  of  a  principle  which,  when  applied,  would 
explain  the  phenomena  in  each  of  the  various  groups  into 
which  the  disorder  has  been  divided.  There  was  abundant 
clinical  experience  showing  the  remedial  effect  on  the 
paroxysm  of  vaso-dilators ;  but  the  only  explanation  of 
the  arterial  spasm  which  up  to  the  present  time  has  been 
offered  has  been,  to  use  Sir  E.  Douglas  Powell's  words,  that  of 
"  a  pure  neurosis  of  the  cardio-vascular  system." 

Owing  to  the  varying  degree  of  intensity  of  the  symptoms, 
I  would  suggest  that  in  classifying  the  cases  the  simplest 
distinction  might  be  found  in  the  terms  "  angina  pectoris 
major "  and  "  angina  pectoris  minor,"  the  former  being 
confined  to  those  cases  in  which  there  was  believed  to  be 
permanent  anatomical  change  in  the  heart  or  its  vessels. 

EEFERENCES. 

G.  A.  Gibson,  Nervous  Affections  of  the  Heart,  1904.  Thomas 
Oliver,  Lancet,  16tli  September  1905,  p.  809.  James  Mackenzie, 
British  Medical  Journal,  7th  October  1905.  Pawlow,  The 
Work  of  the  Digestive  Glands.  Herter,  Lectures  on  Chemical 
Pathology.  Chittenden,  Physiological  Economy  in  Nutrition. 
W.  Heberden,  Med.  Trans.  Col.  of  Phys.,  Lond.,  vol.  ii.  p.  59, 
1772;  do.,  vol.  iii.  p.  1,  1785.  C.  W.  Parry,  An  Inquiry  into  the 
Symptoms  and  Causes  of  the  Syyicojje  Anginosa,  commonly  called. 
Angina  Pectoris,  1799.  Allan  Burns,  Diseases  of  the  Heart,  1809, 
p.  138.  Jurine,  Memoire  sur  I'Angine  de  Poitrine,  1815. 
Laennec,  Diseases  of  the  Chest  (first  edition,  1819),  Eorbes's 
translation,  fourth  edition.  Forbes,  Cycl.  of  Pract.  Med.,  vol.  i., 
1832.  Bertin,  Diseases  of  the  Heart,  etc.,  1833.  Hope,  ^  Treatise 
on  Diseases  of  the  Heart  and  Great  Vessels,  1839.  Latham, 
Diseases  of  the  Heart,  1846.  Walshe,  Diseases  of  the  Heart  (first 
edition,  1851),  third  edition,  1862.  Stokes,  Diseases  of  Heart  and 
Aorta,  1854.  Trousseau's  Lectures  on  Clin.  Med.,  ISTew  Sydenham 
Soc,  vol.  i.  p.  592,  et  seq.  Xothnagel,  Deut.  Arch.  f.  Idin.  Med., 
Bd.  2,  s.  173  ;  Bd.  iii.  s.  309,  Leipzig,  1867.  Sir  B.  C.  Brodie, 
Lectures  on  Pathology  and  Surgery,  1846,  p.  360.  Boullay,  Arch. 
Gen.  de  Med.,  vol.  xxvii.  p.  425,  1831.  Charcot,  Gaz.  Med.  de 
Paris,  1859;  Pr ogres  Med.,  1887,  p.  99.  Lauder  Brunton,  luancet, 
vol  ii.  p.  97,  1867;  Trans.  Clin.  Soc.  Lond.,  vol.  in.  p.  191,  1870. 
W.  T.  Gairdner,  Reynolds's  Sys.  of  Med.,  Lond.  1877,  voL  iv. 
p.  535.  Sansom,  Diagnosis  of  Dis.  of  Heart  and  Aorta,  1892. 
Osier,  Lectures  on  Angina  Pectoris  and.  Allied  Conditions,  1897. 
Sir  R.  Douglas  Powell,  AUbutfs  System  of  Med.,  vol.  vi.     Byrom 

151 


ANGINA  PECTORIS 

Bramwell,  Diseases  of  the  Heart,  1884.  G.  A.  Gibson,  Diseases 
of  the  Heart  and  Aorta,  1898.  George  Oliver,  Blood  Pressure  and 
Tissue  Lymph  Circulation,  1903.  W.  Eussell,  Lancet,  1st  June 
1901  ;  Encii.  Med.,  vol.  xiii.,  "  Vessels  "  ;  British  Medical  Journal, 
4tli  June  1904.  Prof.  Pal,  Gefdsskrisen,  Leipzig,  1905.  Rosen- 
bach,  Die  Kranlclieiten  des  Herzens,  1896.  H.  Hucbard,  Maladies 
du  Coeur,  Tome  2,  1899.  Clifford  AUbutt,  La?ie  Lectures,  1898. 
The  Cavendish  Lecture,  TVest  London  Med.  Journ.,  July  1903. 


152 


CHAPTER   XVI 

THE  PHENOMENA  CAUSED  BY  HYPERTONIC 
CONTRACTION  OR  SPASM  CONSTRICTION  OF 
CEREBRAL    ARTERIES 

Although  physiologists  have  not  located  a  vasomotor  centre 
for  the  cerebral  vessels,  there  are  many  nervous  phenomena 
which  can  only  be  satisfactorily  explained  on  the  assumption 
that  these  vessels  can  and  do  contract.  To  the  clinical  patho- 
logist the  hypothesis  that  tubes  possessed  of  a  muscular  coat 
do  not  respond  to  stimuli,  is  as  improbable  when  it  is 
applied  to  the  cerebral  vessels,  as  it  would  be  if  applied  to 
any  similarly  constituted  structure  in  any  other  part  of 
the  body.  Clinical  medicine  requires  the  recognition  of  such 
contraction.  In  such  circumstances  it  is  usually  found  that 
laboratory  investigation  ultimately  is  able  to  demonstrate 
what  has  been  inferred  from  clinical  phenomena.  It  is,  indeed, 
desirable  to  keep  the  chnical  aspects  of  various  problems 
clearly  defined,  so  that  our  physiological  coadjutors  may 
thereby  be  encouraged  to  continue  thek  very  important 
investigations,  and  perhaps  be  prevented  from  regarding 
questions  as  settled  when  clinical  requirements  are  not 
satisfied. 

It  is  important  and  interesting,  however,  to  remember 
that  all  the  arteries  in  the  body  are  not  connected  with  the 
vasomotor  centre  in  the  medulla.  The  systemic  vessels  and 
the  splanchnic  system  are  linked  to  this  centre,  and  through 
it  have  mutual  relations  with  each  other.  The  vessels  in  the 
brain,  the  coronary  arteries,  and  the  pulmonary  vessels  are 
apparently  not  linked  to  it.  In  this  chapter  attention  is 
confined  to  the  first  of  these,  and  various  clinical  phenomena, 
common  in  clinical  experience,  are  dealt  with.  The  more 
severe  of  these  are  due  to  softening  from  permanent  cutting 

153 


CONTRACTION  OF  CEREBRAL  ARTERIES 

off  of  the  blood  supply  from  portions  of  brain,  while  the  less 
severe  are  unquestionably  clue  to  interference  with  brain 
function,  caused,  I  Ijelieve,  by  local  disturbances  or  alterations 
in  blood  supply  dependent  upon  temporary  and  evanescent 
vessel  changes,  and  in  a  considerable  degree  capable  of 
being  influenced  by  therapeutic  measures.  A  gradual  in- 
tensification in  the  phenomena  referred  to  will  be  found, 
rising  from  transitory  sensations  of  numbness  or  tingling  to 
hemiplegia  and  aphasia.  Many  of  these  phenomena  have 
been  entirely  misunderstood,  because  the  explanation  of  them 
had  not  got  beyond  the  point  of  referring  them  to  the 
vague  category  of  the  "  neuroses."  Any  suggestion  that  the 
phenomena  might  be  vascular  in  origin  was  limited  by  the 
tendency  or  habit  of  thinking  that  all  vessel  phenomena  in 
the  brain  were  embraced  under  either  embolism,  thrombosis, 
or  ha3morrhage.  The  object  of  this  chapter  is  to  show  more 
fully  than  I  have  yet  done,  that  contraction  of  cerebral  vessels 
is  the  direct  or  indirect  cause  of  the  phenomena  referred  to. 
I  have  dealt  with  this  subject  in  papers  already  published,  and 
since  then  it  is  to  be  noted  that  a  few  other  writers  have 
adopted  a  like  view.  In  previous  contributions  to  the  subject  of 
hypertonic  contraction  of  cerebral  vessels,  I  have  dwelt  in  the 
main  on  hypertonus  as  shown  in  sclerosed  vessels ;  that  is,  in 
cases  where  cerebral  manifestations  were  associated  with 
decided  changes  in  the  systemic  vessels.  Here  I  do  not 
confine  myself  to  this  phase,  but  cover  a  wider  field,  so  that 
the  links  in  the  chain  of  evidence  may  be  more  clearly  seen 
to  be  united. 

CEREBRAL  VESSELS,  ALTHOUGH  NOT  CONTROLLED 
FROM  THE  VASOMOTOR  CENTRE,  POSSESS  CON- 
TRACTILITY,  AND   RESPOND   TO    NERVE   STIMULI 

Physiologists  have  shown  that  the  cerebral  vessels  are 
not  under  the  control  of  the  vasomotor  centre  in  the  medulla, 
and,  as  has  been  stated  above,  they  have  not  so  far  found  a 
centre  for  these  vessels  in  any  other  part  of  the  encephalon. 
It  would,  however,  be  very  unsound  to  assume  from  this  that 
cerebral  vessels  have  little  if  any  contractility. 

It  is  of  great  interest,  however,  to  realise  the  significance 

154 


CONTRACTION  OF  CEREBRAL  ARTERIES 

of  the  fact  that,  while  the  great  systemic  system  of  vessels  is 
under  the  control  of  the  vasomotor  centre,  some  local  systems, 
such  as  the  brain,  are  not  so  controlled.  It  was  presumably 
this  fact,  coupled  at  one  time  with  the  failure  to  demonstrate 
nerve  filaments  in  connection  with  cerebral  and  other  vessels, 
which  led  to  the  hasty  conclusion  that  the  muscular  tunic  of 
such  vessels  was  unimportant,  if  not  even  non-essential  or 
unnecessary.  The  acceptance  by  the  physiologists  of  the 
existence  of  nerve  fibres  connected  with  cerebral  vessels  en- 
tirely changes  the  standpoint.  Both  Morrison  and  Gulland 
claim  to  have  demonstrated,  by  the  newer  methods  of 
histological  investigation,  tlie  existence  of  such  filaments ; 
and  this  has  been  accepted  by  so  eminent  a  physiologist  as 
Dr.  Leonard  Hill,  who,  while  stating  at  page  146,  vol.  ii.,  of 
Schiifer's  Physiology  (1900),  that  "no  evidence  has  been 
found  of  the  existence  of  vasomotor  nerves,"  has  added  a 
note  at  page  168,  presumably  as  the  work  was  going  through 
the  press,  granting  the  existence  of  such  cerebral  vasomotor 
nerves.  This  being  so,  it  is  not  necessary  to  labour  the  point 
that  cerebral  vessels  contract  and  dilate,  for  the  possession  of 
a  muscular  coat  and  nerves  in  their  walls  settles  that.  The 
relations  of  these  nerves  have  not,  however,  been  demon- 
strated ;  but,  notwithstanding  this  hiatus,  it  may  be  con- 
fidently assumed  that  nerve  filaments,  here  as  elsewhere,  have 
central  connections.  Although  these  filaments  are  not  con- 
nected with  the  systemic  vasomotor  centre,  they  must  have 
connections  with  other  centres ;  and  it  is  probable,  indeed 
certain,  that  some  of  these  are  with  emotional  centres.  It  is 
accepted  that  emotion  influences  cerebral  function  in  other 
than  emotional  centres,  and  it  is  assumed  from  analogy  that 
it  does  so  by  influencing  local  blood  supply.  It  is  not 
necessary  to  argue  that  local  function  and  local  blood  supply 
go  hand  in  hand.  It  is  equally  unnecessary  to  argue  the 
proposition  that  local  variations  in  blood  supply  must  occur 
in  the  brain ;  and  may  evidently  be  determined  by  causes  not 
acting  upon  the  ordinary  vasomotor  centre,  and  therefore 
showing  no  similar  or  corresponding  changes  in  the  systemic 
vascular  area  controlled  from  that  centre.  While  this  is  true, 
the  converse  must  be  equally  true,  namely,  that  conditions 
which  act  throurjh  the  ordinary  vasomotor  centre  do  not  act 

155 


CONTRACTION  OF  CEREBRAL  ARTERIES 

upon  the  cerebral  circulation.  When  the  point  is  thus  stated, 
and  we  allow  our  minds  to  look  at  it,  and  to  realise  that  the 
separation  of  the  brain  blood  supply  from  the  influence  of 
the  ordinary  vasomotor  centre  must  protect  the  brain  from  a 
multitude  of  influences  which  would  keep  it  in  a  constant 
state  of  instability,  the  arrangement  becomes  a  very  striking 
and  evidently  a  beneficent  one.  That  the  cerebral  vessels 
must  have  a  vasomotor  centre  of  their  own  seems, 
however,  to  be  a  reasonable  inference,  and  perhaps  the 
physiologists  may  yet  be  able  to  locate  it.  Meanwhile,  we 
may  safely  assume  that  the  cerebral  vessels  contract  and  dilate 
under  the  influence  of  certain  nervous  impressions  or  stimuli. 

THE  VESSELS  ACTED  UPON  BY  SUBSTANCES  IN  THE 

BLOOD. 

In  a  previous  chapter  it  has  been  pointed  out  that  a 
number  of  substances  used  therapeutically  act  directly  upon 
tlie  vessel  wall, — that  is,  without  the  medium  of  the  nervous 
mechanism, — leading  to  contraction  or  relaxation  of  its  muscular 
coat.  The  direct  action  of  the  secretions  of  the  adrenal  and 
pituitary  glands  upon  the  vessel  wall  has  also  been  referred 
to  as  adding  weight  to  this  important  and  far-reaching 
proposition.  That  the  secretions  of  these  glands  must  take 
an  important  part  in  determining  vessel  tone,  which  really 
means  the  degree  of  contraction  of  the  muscular  tunic,  seems 
to  be  an  unavoidable  inference,  and  if  this  be  correct  it 
requires  to  be  further  realised  that  the  substances  in  question 
are  probably  present  in  relatively  small  amount  in  the  blood. 
It  is  unthinkable  that  organs  secreting  substances  with  such 
striking  properties  are  not  in  definite,  important,  and  constant 
relations  with  normal  and  ordinary  physiological  everyday 
processes.  It  must,  it  seems  to  me,  be  accepted  as  a  law  that 
vessels  respond  directly  to  the  influence  of  substances  present 
in  the  circulating  blood  even  in  small  quantity. 

THE   APPLICATION   OF   THE   FOEEGOING   TO    THE 
CEREBRAL   VESSELS. 

From  the  foregoing  it  is  evident  that  we  are  entitled  to 
formulate    and   to   hold   the   following  four    important    pro- 

156 


IxNFLUENCE  OF  BLOOD  COMPOSITION 

positions,  namely :  first,  that  vessels  possessing  a  muscular 
coat  must  be  regarded  as  capable  of  contracting  and  dilating, 
although  not  connected  with  the  systemic  vasomotor  centre ; 
second,  that  it  has  been  experimentally  proved  that  the 
contraction  of  vessels  may,  be  effected  by  the  direct  action 
on  their  walls  of  substances  circulating  in  them,  acting 
without  the  intervention  of  the  nervous  mechanism,  and 
present  in  small  quantity ;  third,  that  the  phenomenon  of 
vessel  constriction  is  not  necessarily  present  in  all  parts  of 
the  body  simultaneously,  but  can  be  manifested  locally ;  and 
fourth,  that  these  propositions  must  be  applicable  to  the 
cerebral  vessels. 

The  two  influences  which  affect  the  degree  of  tone,  con- 
traction, or  constriction  of  vessels  are  therefore  nervous 
influences  and  blood  composition ;  and  this  must  be  true  of 
the  cerebral  as  it  is  of  the  systemic  vessels. 

Nerve  Influence. — The  effect  of  nerve  influences  is  seen 
in  the  result  of  emotion  on  cerebral  activity — it  may  exalt  or 
depress,  it  may  open  wide  the  gates  of  speech,  or  it  may 
cause  a  temporary  loss  of  utterance.  All  similar  and  allied 
phenomena  must  be  held  as  associated  with  focal  modifications 
of  blood  supply,  and  consequently  with  a  degree  of  local 
vessel  constriction.  This  is  our  conception  of  brain  function 
and  its  attendant  blood  supply.  I  need  only  quote  one 
readily  available  physiological  support  to  this,  which  states 
that  in  the  cerebral  vessels  "  there  is  to  be  recognised  a 
movement  of  vascular  elevation  and  depression  occurring 
from  twice  to  six  times  in  a  minute,  corresponding  to  the 
periodic-regulatory  dilatation  and  contraction  of  the  vessels." 
It  is  further  stated  that  "  this  movement  is  influenced  by 
emotional  disturbances." 

Influence  of  Blood  Composition. — The  direct  influence 
on  the  vessel  wall  of  substances  circulating  in  the  blood  has 
been  so  fully  established,  that  it  is  only  necessary  to  lay 
emphasis  on  the  statement  that  the  facts  must  be  applicable 
to  the  cerebral  vessels.  Whatever  difficulty  there  may  have 
been  in  the  past  regarding  the  cerebral  vessels  in  relation  to 
nerve  impulses,  it  is  impossible  to  exclude  the  cerebral,  or 
any  other  group  of  vessels,  from  the  influence  of  blood  com- 
position.     And  I  venture    to    suggest  that  it  has  been   the 

157 


CONTRACTION  OF  CEREBRAL  ARTERIES 

non-recognition  of  this  fact  which  has  given  rise  to  in- 
accurate and  misleading  teaching. 

Effect  of  Strychnine. — There  is,  it  seems  to  me,  a  large 
and  important  field  in  connection  with  the  cerebral  vessels 
ready  for  investigation.  As  warranting  this  statement,  I 
may,  using  the  authority  above  referred  to,  point  out  that 
strychnine  irritates  the  systemic  vasomotor  centre  leading  to 
constriction  of  vessels,  while  there  is  at  the  same  time  an 
increase  in  the  amount  of  blood  in  the  arteries  of  tlie  central 
nervous  system.  ■  This  shows  that  the  latter  do  not  parti- 
cipate in  the  contraction ;  that,  in  fact,  this  substance  has  a 
different  action  upon  the  cerebral  vessels  to  what  it  has  on 
the  systemic  vessels,  presumably  because  it  acts  through  the 
systemic  vasomotor  centre,  and  not  directly  on  vessel  walls. 

The  Relation  of  the  Pituitary  Body  to  the  Cerebral 
circulation. — This  field  for  investigation  seems  to  me  to  be 
even  more  interesting  than  the  foregoing  suggests.  It  has 
been  shown  that  the  hypophysis  of  the  pituitary  body  has 
much  the  same  constrictor  influence  on  the  vessels  as  the 
adrenal.  It  seems  to  me  unreasonable  to  regard  the  pituitary 
hypophysis  as  a  mere  supernumerary  of  the  adrenals,  and  yet 
I  have  not  seen  it  suggested  that  the  former  may  have  any 
special  relationship  to  the  cerebral  circulation.  And  yet 
what  would  be  more  reasonable  or  more  in  conformity  with 
much  of  our  more  recently  acquired  knowledge  of  the  relation 
of  structure  to  function  ?  Seeing  that  the  cerebral  circulation 
has  a  considerable  measure  of  local  autonomy,  it  is  but 
reasonable  to  expect  that  this  special  structure  is  present 
where  it  is  to  facilitate  the  working,  or  even  as  necessary  to 
the  realisation  of  this  autonomy.  Although  both  glands 
have  a  similar  action,  reference  has  already  been  made  to 
Haynes'  work,  which  shows  that  there  is  a  difference  between 
them  whicli  is  both  interesting  and  suggestive.  In  the  series 
of  experiments  with  ergot,  dealt  with  in  a  previous  chapter, 
he  has  shown  that  large  doses  of  ergot  (which  have  the 
reverse  effect  of  small  doses)  abolish  the  action  of  adrenal 
extract,  while  they  do  not  so  act  upon  pituitary  extract. 
Large  doses  of  ergot  also  lead  to  loss  of  sympathetic  nerve 
action,  so  that  ergot  has  a  corresponding  effect  upon 
sympathetic  and  adrenalin  action.      It  has,  however,  no  such 

158 


CLINICAL  APPLICATION 

action  upon  the  pituitary,  the  cerebral  analogue  of  the 
adrenal ;  and  the  cerebral  circulation  is  also  outside  the 
systemic  vasomotor  system.  The  conditions  which  regulate 
the  activity  of  the  pituitary  are  as  little  known  as  those 
vi^hich  determine  adrenal  activity,  but  it  will  not  be 
questioned  that  Haynes'  findings  are  highly  suggestive,  and 
suggest  subtleties  the  investigation  of  which  by  physiologists 
might  place  most  valuable  measures  in  the  hands  of  the 
clinician.  Garnier  and  Thaon  have  shown  that  when  the 
vagus  is  cut  the  pituitary  hypophysis  has  no  effect  on  the 
blood -pressure. 

Clinical  Application. — It  appears  from  the  foregoing  that 
we  are  abundantly  justified  in  requisitioning  cerebral  vessel 
contraction  for  clinical  purposes,  and  also  in  holding  that  the 
state  of  the  systemic  is  in  some  cases  a  guide  to  the  state  of 
the  cerebral  vessels,  while  in  other  cases  it  is  not  a  guide. 
Tliis  being  the  position,  it  must  be  further  assumed  that  the 
vessels  in  localised  ond  circumscribed  areas  of  brain  can  be 
affected  without  a  like  and  simultaneous  involvement  of  the 
entire  intracranial  circulation.  Such  a  proposition  is,  in 
view  of  the  anatomical  and  physical  conditions,  incapable  of 
ocular  demonstration ;  but  even  here  we  are  not  without 
cognate  facts  which  warrant  us  in  accepting  it.  It  is  well 
known  that  local  vessel  constriction  is  an  accompaniment  of 
migraine,  and  that  relief  of  suffering  accompanies  vessel 
relaxation.  It  has  also  been  noted  that  spasm  of  retinal 
vessels  may  occur  in  Eaynaud's  disease.  Dr.  Lunelle  recorded 
a  case  recently  in  which  he  contended  that  temporary 
blindness  was  due  to  spasm  of  retinal  vessels,  the  blindness 
passing  off  when  the  constricted  vessels  relaxed.  In  the 
argument  in  support  of  his  contention  regarding  the  cause  of 
the  temporary  blindness  in  his  own  patient,  he  refers  to  other 
observations  of  the  same  kind  in  which  both  generalised  and 
limited  constriction  of  retinal  vessels  had  been  noted. 
When  the  constriction  is  limited,  the  area  of  l^lindness 
corresponds  with  the  position  of  the  constricted  branch. 
Lundie's  interesting  paper  brings  together  sufficient  facts  to 
prove  that  temporary  constriction  may  occur  in  all  or  some 
of  the  branches  of  the  retinal  artery,  and  my  contention  has 
been  that  corresponding  processes  occur  in  the  brain.      That 

159 


COxNTRACTION  OF  CEREBRAL  ARTERIES 

they  occur  in  the  retinal  vessels  gives  strong  support  to  my 
contention,  and  I  hold  may  be  claimed  to  be  as  near  absolute 
proof  as  is  attainable. 

I  have  arranged  the  cases  showing  symptoms  which  I 
hold  to  be  the  outcome  of  vascular  disturbance  in  the  brain, 
into  groups  illustrating  the  degrees  of  importance  of  the 
symptoms.  The  groups  also  show  a  gradation  of  links  which 
strengthens  the  contention  that  the  cases  have  the  same 
underlying  clinical  pathology. 

The  patients,  showing  the  symptoms  referred  to,  can  be 
divided  into  two  main  classes ;  namely,  those  whose  vessels 
were  sclerosed,  and  those  whose  vessels  were  not  per- 
manently thickened.  In  the  different  groups  both  classes  may 
be  included. 

GEOUP    I. — TKANSITORY   PHENOMENA  :    SLIGHT   AND 

GRAVE. 

I  begin  with  the  cases  showing  minor  and  transitory 
phenomena,  minor  when  occurring  in  persons  with  soft 
vessels ;  of  much  more  grave  significance  when  occurring  in 
persons  with  thickened  vessels.  In  the  second  class  the 
symptoms  are  commonly  and  justly  regarded  as  premonitory 
of  apoplexy. 

Accompaniments  of  Migraine. — It  is  not  necessary  to 
dwell  upon  the  association  of  migraine  with  arterial  con- 
traction, for  it  is  widely  known  and  recognised.  Not  only 
that,  but  Thoma  states  that  he  has  seen  a  case  of  supra-orbital 
neuralgia  followed  by  thickening  of  the  temporal  artery,  on 
the  side  attacked  by  the  pain,  the  result  of  the  recurring 
spasm.  It  is  also  well  known  that  various  visual  phenomena 
may  be  associated  with  an  attack,  the  most  striking  being 
a  homonymous  hemianopsia  on  one  or  other  side.  When 
recently  talking  over  this  aspect  of  my  subject  with  Mr.  E. 
Marcus  Gunn,  F.R.C.S.,  Senior  Ophthalmic  Surgeon  at 
Moorfields  Hospital,  London,  he  informed  me  that  he  knew 
of  cases  of  migraine  which  w^ere  accompanied  with  various 
defects  of  speech,  such  as  partial  or  complete  motor  aphasia, 
a  measure  of  amnesia,  or  a  degree  of  paraphasia.  He  also 
knew  of  sensory  phenomena  referred  to  one  side  of  the  body, 

1 60 


CASES  ILLUSTRATING  TRANSITORY  PHENOMENA 

of  hemiparesis,  or  of  brachial  monoparesis.  These  various 
accompaniments  coincided  with  the  attack  of  migraine,  and 
disappeared  with  its  subsidence.  Assuming  the  view  of  the 
relation  between  migraine  and  local  arterial  spasm  to  be 
correct,  and  personally  I  do  not  doubt  it,  it  is  legitimate  to 
infer  that  the  additional  phenomena  are  the  result  of  a 
corresponding  spasm  in  the  areas  of  brain  to  which  they  are 
referable. 

Cases  illustrating  Transitory  Phenomena. 

Case  60  was  a  young  medical  graduate,  who  informed 
me  that  when  he  was  working  hard  and  much  run  down 
in  condition  he  had  an  attack  of  complete  loss  of  speech 
and  of  power  in  the  right  arm.  The  condition  after 
lasting  for  an  hour  passed  off.  He  was  subject  to  attacks 
of  migraine,  and  it  was  thought  that  this  seizure  was  a 
"  migrainous  manifestation."  He  himself,  in  the  light  of 
my  published  views  on  hypertonic  contraction  of  arteries, 
had  come  to  regard  the  attack  as  illustrating  and  confirming 
my  contentions.  This  case  corresponds  with  the  cases 
referred  to  in  the  preceding  paragraph. 

Case  61  was  a  medical  friend  in  middle  life,  who  on 
getting  out  of  bed  one  morning  had  a  sensation  of  numbness 
on  the  left  side  of  his  body,  including  his  face.  He  could 
move  his  limbs  and  stand,  but  his  limbs  felt  as  if  they  did 
not  belong  to  him.  The  attack  passed  off  in  a  few  minutes. 
The  arteries  were  soft. 

Case  62. — A  gentleman,  ast.  69,  consulted  me  regarding 
a  recurring  feeling  of  numbness  in  the  right  arm,  which  came 
and  went  without  any  cause  so  far  as  he  could  see.  He  had 
a  feeble  circulation,  and  a  tendency  to  slight  hypertonic  con- 
traction of  his  vessels.  I  gave  him  a  pill  containing  iron  and 
digitalis,  and  a  mixture  containing  10  minims  of  sp.  etheris 
nitrosi  in  each  dose,  with  instructions  to  take  a  dose  when- 
ever he  felt  the  sensation  referred  to.  He  was  quite  confident 
that  the  ether  gave  him  speedy  relief,  and  he  soon  ceased  to 
experience  the  unpleasant  sensation  mentioned. 
L  i6i 


CONTRACTION  OF  CEREBRAL  ARTERIES 

Case  63. — A  man,  set.  63,  consulted  me  at  the  Eojal 
Infirmary  on  Wednesday,  30th  May  1906.  He  stated  that 
on  the  previous  Saturday  he  completely  lost  the  power  of 
speech  for  an  hour  or  two,  but  regained  it  fully  before  night. 
When  he  awoke  on  Sunday  morning  his  whole  left  side  was 
powerless,  and  his  face  was  twisted  to  the  right.  Power  had 
returned  to  the  arm  and  leg  sufficiently  to  permit  him  to 
walk  to  the  Infirmary.  When  he  presented  himself  there, 
he  still  showed  a  little  feebleness  of  the  limbs  on  the  left  side, 
and  the  face  was  drawn  to  the  right  side.  There  was  no 
loss  of  sensibility.  The  radial  arteries  were  markedly 
thickened,  but  there  was  no  albumin  in  the  urine.  There 
had  been  no  loss  of  consciousness. 

Case  64. — A  man,  pet.  48,  was  seen  by  me  on  Monday, 
31st  December  1906.  His  statement  was  that  on  Saturday 
morning  about  8.45,  when  lying  in  bed  before  having  break- 
fast, but  an  hour  after  having  had  a  cup  of  tea,  a  feeling 
as  of  pins  and  needles  began  in  his  left  ankle,  spread  up  his 
lesf,  the  left  half  of  his  trunk  to  the  shoulder,  and  down  the 
left  arm.  It  was  not  in  the  neck  or  face.  His  arm  became 
"  cold  and  useless  "  :  he  could  move  the  arm  but  it  felt  useless, 
and  he  could  not  grip  the  bedclothes  with  his  hand.  He 
did  not  try  his  leg.  In  about  half  an  hour  this  passed  off 
slowly,  and  he  "  felt  the  heat  gradually  coming  back."  On 
Sunday  morning  (the  day  before  I  saw  him)  about  a  quarter 
to  nine  he  had  begun  breakfast  in  bed  and  wanted  to 
speak  to  his  wife,  but  could  not  speak,  "  could  only  make  a 
noise,"  and  "  get  no  words  out."  He  stopped  taking  break- 
fast and  lay  quiet.  About  10.30  speech  returned,  but  it 
was  "  kind  of  stumbling  "  all  day — "  like  a  man  that  stutters." 
On  Monday  morning  he  was  all  right.  He  had  been  confined 
to  the  house  from  the  preceding  Monday  with  "  a  cold " 
(influenza).  There  was  no  albumin  in  the  urine.  The  radials 
were  slightly  hypertonic,  the  pulse  was  feeble,  and  the  heart 
sounds  faint.  He  had  some  other  attacks  and  came  into  my 
ward  in  the  Eoyal  Infirmary  on  7  th  January.  He  was  kept 
in  bed  and  given  liquor  strychninie  and  tincture  of  squill.  He 
had  three  attacks  of  a  "  prickly  feeling  "  in  his  left  side,  and 
one  which  he  described  as  a  "  dragging,"  "  like  leather  which 

162 


CASES  ILLUSTRATING  TRANSITORY  PHENOMENA 

had  been  wet  and  then  was  drying."  The  pnlse  ranged 
between  78  and  84  or  so.  The  hsemomanometer  on  three 
different  days  gave  readings  of  105°— 95°  and  100°.  The 
pulse  was  soft  and  feeble.  He  went  home  on  tlie  15th,  and 
reported  himself  at  the  ward  on  the  10th,  and  was  advised  to 
continue  his  medicine. 

Case  65. — Thomas  N.,  cet.  68,  army  pensioner,  stated 
that  on  Saturday,  loth  December  1906,  he  had  been  out 
walking  about  as  usual.  On  the  following  day  when  he  got 
out  of  bed  he  had  a  feeling  of  numbness  in  the  left  side  of  his 
face  and  the  left  arm  and  leg.  I  saw  him  at  Queensberry 
House  on  the  following  Wednesday,  the  19th,  when  he  com- 
plained of  a  feeling  of  numbness  and  '•'  stiffness  "  in  his  whole 
left  side,  and  thought  it  was  "  rheumatic "  and  due  to  a 
"  heavy  cold."  The  condition  had  become  worse  since 
Sunday,  and  he  felt  that  he  was  dragging  the  left  leg  more. 
He  could  move  the  left  arm  and  hand,  but  he  could  not  grasp 
my  hand ;  he  could  just  close  his  fingers  on  my  hand.  He 
had  been  moving  about  since  Sunday,  but  he  dragged  the  left 
leg  a  little.  The  face  was  drawn  slightly  to  the  right,  there 
being  distinct  paresis  of  the  left.  Speech  was  not  affected, 
but  he  became  emotional  when  I  told  him  he  must  go  to  bed. 
I  sent  him  to  my  ward  in  the  Infirmary.  When  examined 
in  l^ed,  in  addition  to  the  foregoing  facts,  it  was  found  that 
sensibility  to  pinching  was  diminished  and  delayed  on  the 
left  side.  The  knee  jerk  was  absent  on  both  sides.  The 
plantar  reflexes  were  not  elicited  by  tickling  the  soles,  but  on 
deep  pressure  the  right  was  much  more  active  than  the  left. 
There  was  no  Babinsky.  The  pulse  was  66,  the  artery 
somewhat  thickened,  Oliver's  hgemomanometer  recorded  a 
pressure  of  165.  He  was  given  half  a  grain  of  erythrol 
tetranitrate  every  four  hours.  On  the  20  th,  he  was  given, 
in  addition,  5  minims  tinct.  digitalis  every  four  hours,  which  was 
reduced  to  3  minims  on  the  21st,  as  it  had  tightened  his  vessels; 
and  as  this  effect  was  still  more  marked  on  the  22nd,  it  was 
stopped,  and  the  erythrol  was  given  every  three  hours,  and 
in  addition  5  grains  of  potassium  iodide  were  given  three 
times  a  day.  On  the  21st,  the  patient  could  draw  up  and 
extend  the  leg  against  considerable  obstruction ;  no  response 

163 


CONTRACTION  OF  CEREBRAL  ARTERIES 

to  tickling  the  soles ;  deep  pressure  gave  marked  reaction 
on  right  side,  but  very  faint  on  left.  On  the  22nd,  the  grasp 
of  the  hand  was  a  little  stronger.  On  the  26th,  the  grasp  of 
the  hand  had  further  increased.  On  the  27th,  erythrol  was 
stopped,  iodide  of  potassium  was  continued,  and  he  was  given 
in  addition  5  minims  of  liq.  strychnine  hydrochloridi  three  times 
a  day.  On  the  30th,  he  moved  his  left  hand  and  arm  freely, 
and  said  that  they  felt  "quite  well":  the  grasp  of  the  hand 
was  strong.  There  was  still  paresis  of  the  left  side  of  the 
face.  The  reflex  to  tickling  the  soles  was  prompt  and  equal 
on  the  two  sides.  There  was  no  dragging  of  the  foot  when 
walking.  The  radial  artery  on  the  29  th,  as  well  as  on  the 
30th,  was  soft,  all  trace  of  thickening  having  disappeared. 
There  was  more  colour  in  the  face :  at  first  his  face  was  pale 
and  somewhat  pinched,  now  it  was  slightly  ruddy.  The 
hccmomanometer  gave  a  reading  of  120.  He  was  allowed 
to  go  out  on  the  31st.  I  saw  him  on  the  18th  of  January, 
when  he  confidently  asserted  that  his  arm  and  leg  were  "  all 
right,"  but  the  left  side  of  his  face  had  not  made  any  further 
measure  of  recovery,  and  he  complained  of  his  food  gathering 
Ijetween  his  cheek  and  gum  on  that  side.  This  man  had 
remained  well  when  this  went  to  press  in  the  middle  of 
September  1907. 

Remarks. — When  the  subsequent  groups  of  cases  are 
followed,  it  will  be  seen  that  the  cases  in  this  group  divide 
themselves  into  the  two  classes  already  indicated, — the  less 
grave  cases  being  represented  by  the  victims  of  migraine,  in 
whom  the  symptoms  are  usually  well  under  medical  control, 
and  the  prognosis  correspondingly  satisfactory.  The  grave 
cases  are  those  in  which  the  symptoms  are  associated  with 
vessel  thickening,  or  occur  in  old  people  with  soft  vessels  and 
a  feebly  acting  heart.  The  gravity  of  these  latter  cases  lies 
in  the  risk  of  cerebral  softening  taking  place,  the  steps  which 
lead  to  such  a  disaster  are  discussed  later. 

These  cases  lead  to  a  second  group  in  which  there  was 
recurring  mental  or  motor  phenomena.  In  this  group  there 
is  probably  always  arterial  disease. 


164 


RECURRING  MENTAL  OR  MOTOR  PHENOMENA 

GROUP   II. — RECURRING   MENTAL   OR    MOTOR 
PHENOMENA. 

In  this  group  I  include  a  number  of  cases,  which  ilkistrate 
the  considerable  variety  of  clinical  phenomena  which  may  be 
encountered,  and  the  significance  of  which  it  is  desirable  not 
to  misapprehend  in  practice.  I  begin  the  group  with  a 
retired  military  man. 

Case  66,  set.  70  years,  had  thickened  arteries,  and  marked 
arcus  senilis.  There  was  no  albumin  in  the  urine.  He  com- 
plained of  having  become  unusually  somnolent  after  lunch  and 
dinner  ;  his  speech  had  become  a  little  thick  and  blurred  ;  l^ut 
what  annoyed  him  most  was  that  he  had  begun  to  spell  words 
incorrectly  in  his  letters,  a  thing  he  had  never  done  before ; 
his  gait  had  also  become  slightly  unsteady.  In  fact,  his  condi- 
tion at  the  time  to  which  I  refer,  which  was  some  years  before 
he  died,  was  such  as  to  suggest  rapid  cerebral  degeneration.  I 
was,  however,  satisfied  that  the  symptoms  were  due  to  hyper- 
tonus  of  his  sclerosed  vessels  curtailing  the  brain  blood 
supply.  I  knew  that  in  eating  and  drinking  he  was  very 
moderate,  as  judged  by  ordinary  standards,  yet  after  careful 
consideration  I  strongly  advised  him  to  give  up  the  glass  of 
claret  he  took  at  lunch  and  dinner.  He  at  once  fell  in  with 
my  advice ;  and  was  rewarded  by  the  disappearance  in  a  very 
short  time  of  the  symptoms  which  had  given  us  so  much 
concern.  Along  with  the  improvement  there  was  a  definite 
arterial  relaxation.  I  mention  this  case  because  it  is  illustra- 
tive of  a  type.  There  was  a  very  marked  readiness  on  the 
part  of  the  arteries  to  tighten  up  a  little,  and  for  long  periods 
a  small  quantity  of  potassiuni  iodide  was  sufficient  to  control 
it.  After  the  continuance  of  such  a  period  there  would  be 
some  deviation  from  the  ordinary  austerity,  some  extra  proteid 
added  to  the  dietary,  or  some  small  measure  of  alcoholic  fluid 
taken  at  lunch  or  dinner,  and  as  sure  as  this  occurred  there 
was  a  threatening  of  the  former  symptoms,  and  an  appreciable 
hypertonic  tightening  up  of  his  radial  arteries.  The  total 
quantity  of  proteid — and,  indeed,  of  every  kind  of  food  taken 
—was  relatively  small ;  and  the  same  was  true  of  the 
amount  of  wine  or  of  spirit.      A  more  regular  and  temperate 

165 


CONTRACTION  OF  CEREBRAL  ARTERIES 

man  could  hardly  be  found,  and  yet  he  was  constantly 
threatened  with  dangers  more  associated  with  the  opposite 
habit.  How  is  a  patient  of  this  kind  to  be  looked  at  ?  Are 
we  to  be  content  to  regard  him,  as  is  not  unusual,  merely  as 
an  old  man  whose  "  strength "  has  to  be  kept  up  ?  This 
view,  when  acted  upon,  ends  speedily  in  disaster.  I  submit 
that  this  man  showed  in  later  life  in  a  concrete  form  what  had 
been  his  physiological  standard  during  life.  There  was  in 
him  a  physiological  barrier  to  his  being  a  large  feeder  or  a 
big  drinker.  We  all  know  such  persons — persons  who 
cannot  eat  big  dinners  daily,  or  take  alcoholic  liquor  of  any 
kind  regularly  save  in  small  quantity.  The  barrier  is  really 
a  physiological  one ;  the  organs  concerned  are  not  capable 
of  dealing  with  the  amount  or  kind  of  work  thrown  upon 
them,  and  auto- intoxication  or  toxaemia  of  one  kind  or 
another  results. 

Case  67.^ — This  case  illustrates  a  type  of  symptom  common 
in  old  people  w^ith  thickened  vessels,  physical  weakness,  and 
the  deteriorated  brain,  so  frequently  regarded  as  the  inevitable 
result  of  senility. 

Such  persons  from  time  to  time  are  seized  with  restlessness, 
insomnia,  mental  excitement,  which  amounts,  during  the 
night,  to  a  form  of  delirium.  They  get  out  of  bed  during  the 
night  and  wander  about  the  room  if  allowed  to  do  so,  or  do 
strange  and  dangerous  things,  as  lighting  matches,  and 
interfering  with  the  fire.  When  an  attack  of  this  kind  is  on, 
I  always  find  that  their  sclerosed  arteries  have  undergone 
marked  contraction.  I  had  some  time  ago,  in  the  male  sick 
ward  of  Queensberry  House,  a  very  pretty  example  of  this 
condition.  The  patient  was  a  very  old  man,  but  usually 
quiet  and  inoffensive,  sleeping  well,  and  moving  about  during 
the  day,  giving  no  trouble  to  anyone.  When  his  attack 
came  on  he  w^as  as  I  have  described.  The  striking  feature, 
beyond  the  manifestations  I  have  mentioned,  was  a  remark- 
able contraction  of  his  arteries.  The  radials,  which  were 
always  somewhat  sclerosed,  but  of  good  size,  with  a  fair 
volume  of  blood  in  them,  become  redi\ced  by  contraction  to 
half  their  ordinary  size  or  even  less.  The  infallible  remedy 
for  these  attacks  in  this  old  man  was  a  dose  of  paraldehyde. 

166 


RECURRING  MENTAT.  OR  MOTOR  PHENOMENA 

If  this  was  given  at  night  he  slept  quietly,  and  next  morning 
his  arteries  had  returned  to  their  ordinary  condition.  With 
a  few  days  of  very  low  diet,  and  sometimes  a  second  dose  of 
paraldehyde,  he  returned  to  his  ordinary  condition.  No  other 
hypnotic  or  sedative  had  the  effect  upon  his  arteries  that 
paraldehyde  had,  and  no  other  had  any  beneficial  effect  upon 
his  attacks.  This  drug  does  not  have  a  corresponding  effect 
upon  all  such  cases.  In  other  cases  the  hypertonus  which 
leads  to  the  insomnia  and  restlessness  can  be  counteracted  by 
means  of  laxatives,  or  by  sulphonal,  trional,  veronal,  oi 
phenacetin.  or  by  a  combination  of  two  of  these.  The 
explanation  of  arterial  contraction  causing  this  train  of 
symptoms  is  to  be  found  in  the  anaemia  of  an  enfeebled  and 
degenerated  brain — the  anaemia  being  due  to  the  vessel 
constriction ;  and  the  symptoms  disappear  as  the  constriction 
is  removed. 

Case  68.— Mrs.  M.,  at.  72,  who  had  been  for  years 
an  inmate  of  Queensberry  House.  On  Sunday,  14th  October 
1906,  she  had  a  gastric  attack,  wdth  sickness  and  vomiting. 
Under  treatment  these  symptoms  disappeared,  but  on  Tuesday 
she  was  mildly  delirious,  with  delusions.  On  Thursday 
morning  she  had  complete  aphasia  and  right  hemiplegia  ; 
but  gave  her  left  hand  when  asked,  and  in  other  ways 
showed  she  was  conscious.  She  was  seen  shortly  after 
the  onset  of  these  symptoms  and  was  ordered  erythrol 
tetranitrate.  On  Friday  the  dose  was  increased.  She 
rapidly  improved,  and  in  the  course  of  a  few  days  regained 
the  power  of  speech  to  a  considerable  extent,  whilst  the 
paralysis  of  the  limbs  as  steadily  passed  off.  Within  a  fortnight 
she  was  walking  about  as  formerly  and  speaking  distinctly. 

This  patient  had  another  attack  of  delirium  in  April  1907, 
with  slight  motor  enfeeblement  on  the  right  side,  while  the 
speech  became  inarticulate.  As  the  result  of  our  former 
experience  of  her,  the  bowels  were  at  once  freely  cleared  out, 
and  she  w^as  sriven  trional  at  night.  She  was  less  restless, 
although  she  only  slept  for  two  or  three  hours,  but  the  paresis 
was  less.  She  then  got  thirty  minims  of  paraldehyde,  after 
which  she  had  a  whole  night's  sleep,  and  the  paresis  was 
entirely  gone,  although  the  speech,  while  distinctly  improved, 

167 


CONTRACTION  OF  CEREBRAL  ARTERIES 

was  still  indistinct.  The  two  following  nights  she  slept 
soundly  without  a  hypnotic. 

As  the  outcome  of  observations  on  this  patient,  it  was 
found  that  at  short  intervals  she  became  restless,  excited, 
and  wakeful  during  the  night.  "When  the  first  trace  of  these 
symptoms  appeared,  she  was  given  two  grains  of  calomel  and 
a  small  dose  of  castor  oil  at  bedtime,  with  the  result  that  she 
was  quiet  and  composed  the  following  day.  In  the  month  of 
June  after  this  course  had  been  followed  for  some  time,  I  took 
a  hsemomanometer  observation  on  the  forenoon  of  the  evening 
she  was  to  be  given  the  usual  dose,  and  found  it  140  mm. 
Hg.,  and  the  pulse  7  2  ;  the  following  forenoon  it  was  125  mm. 
Hg.,  and  the  pulse  was  80  and  larger. 

On  July  24th,  1907,  when  dressing  in  the  morning,  the 
right  hand  began  to  shake,  and  then  the  whole  right  side.  She 
was  at  once  undressed  and  put  to  bed.  I  saw  her  soon  after, 
and  found  her  in  a  dazed  condition,  and  not  able  to  answer  the 
questions  addressed  to  her.  She  evidently  could  not  speak  ; 
the  right  arm  and  leg  were  paralysed,  but  both  limbs  were 
jerking  rhythmically.  There  was  no  response  on  the  right 
side  to  tickling  the  sole  of  that  foot  ;  but  tickling  the  right 
caused  as  active  a  response  on  the  left  side  as  when  the  left 
sole  was  tickled.  She  was  given  quarter  of  a  grain  of  erythrol 
tetranitrate  every  four  hours.  The  next  forenoon,  as  soon  as 
I  appeared  at  her  bedside,  she  raised  herself  into  a  sitting 
posture,  answered  questions  promptly,  and  gave  me  her 
right  hand.  The  nurse  informed  me  that  the  jerking  of 
the  limbs  ceased  soon  after  the  first  dose  of  the  erythrol  was 
given.  Between  the  25  th  and  the  31st  the  manometer 
pressures  seemed  to  be  very  erratic,  ranging  between  140 
and  170  mm.  Hg.,  but  finally  settled  down  to  about  130. 

This  leads  to  the  third  group  in  which  paralysis  or  paresis 
became  permanent  after  having  been  preceded  by  "  warning 
attacks." 


GROUP   III. — PERMANENT   PARALYSIS   OR   PARESIS 
PRECEDED   BY   "WARNING   ATTACKS." 

Case   69. — J.   F.,  set.   72,  was  seized,  on   5th  February 
1907,  with  slight  paresis  of  the  right  side,  and  of  the  right 

1 68 


PERMANENT  PARALYSIS  OR  PARESIS 

side  of  the  face,  and  slight  impairment  of  speech.  He 
completely  recovered  the  power  in  the  arm  and  leg,  but 
speech  continued  to  be  a  little  blurred,  and  the  facial  paresis 
persisted.  In  June  he  had  another  attack  of  feebleness  on 
the  same  side,  with  a  corresponding  increase  of  the  difficulty 
in  speaking.  Even  after  this  second  attack  he  was  able  to  be 
out  of  iDcd,  could  walk  across  his  room,  and  could  articulate 
well  enough  to  be  understood.  Mentally  he  was  alert  and 
cheerful.  On  6  th  September  he  had  complete  left  hemiplegia 
and  could  not  speak  a  word.  In  various  ways  it  was  seen 
that  he  was  quite  conscious.  I  admitted  him  to  the  Infirmary 
the  same  day,  and  kept  him  under  observation  for  a  fortnight. 
At  the  end  of  that  time  the  leg  had  regained  a  little  power  of 
movement,  and  occasionally  he  spoke  a  word  or  two,  but  he 
could  not  answer  simple  questions.  In  this  condition  he  is 
likely  to  remain.  The  hsemomanometer  observations  made 
on  this  patient  are  referred  to  in  previous  chapters,  so  I  do 
not  repeat  them  here. 

Case  70. — Mrs.  C,  a;t.  77,  when  returning  home  in  the 
afternoon  of  8th  February  1907,  went  into  a  shop  with  the 
purpose  of  making  a  purchase,  but  could  not  tell  the  shopman 
what  she  wanted.  She,  however,  was  able  to  point  to  the 
article  wanted.  I  saw  her  the  following  day,  and  found  that 
she  had  a  very  interesting  type  of  aphasia,  the  details  of  which 
need  not  be  entered  upon  here.  I  admitted  her  to  my  ward 
in  the  Infirmary,  where  her  type  of  aphasia  was  demonstrated 
to  a  number  of  medical  men.  For  our  present  purpose  it  is 
sufficient  to  say  that  beyond  the  speech  difficulty  there  was 
no  symptom.  There  was  no  paresis  of  the  limbs  or  face. 
She  improved  considerably,  but  there  remained  a  measure 
of  word  difficulty.  After  a  time  she  moved  about  as  she  had 
previously  done,  and  went  out  freely.  On  the  morning  of 
the  25th  July  1907,  she  had  got  out  of  bed  and  dressed 
herself  as  usual,  when  s]ie  suddenly  felt  giddy,  and  as  if  she 
were  to  fall.  She  sat  down  on  a  chair,  and  was  helped  to 
bed.  I  saw  her  about  an  hour  afterwards,  and  found  that  she 
had  left  hemiplegia,  the  left  side  of  the  face  being  also 
affected.  She  was  quite  sensible,  and  talked  volubly,  as  w^as 
her  custom.     The  word  defect  was  not  appreciably   greater. 

169 


CONTRACTIOxN  OF  CEREBRAL  ARTERIES 

On  stroking  the  left  sole  there  was  marked  dorsiflexion 
of  all  the  toes,  while  a  similar  proceeding  on  the  right 
side  caused  plantar  flexion  of  all  the  toes.  There  was  no 
loss  of  sensibility.  The  pulse  was  68,  and  the  arterial 
pressure  185  mm.  Hg.  Some  observations  were  made  by 
means  of  the  hsemomanometer  applied  in  the  usual  way,  and 
also  by  means  of  Oliver's  hffimodynamometer  applied  to  the 
temporal  artery,  which  was  thickened  and  lent  itself  to  such 
observations.  There  was  a  difference  of  20  mm.  Hg.  between 
the  two.  Some  improvement  took  place  in  the  leg  in  this 
patient,  but  beyond  that  there  is  nothing  to  record. 

Case  71. — Mr.  H.,  tet.  57,  was  seen  with  Dr.  Inkster. 
The  history  was  that  sixteen  months  before  I  saw  him  he 
was  seized  with  complete  aphasia,  when  in  his  office,  while  at 
the  same  time  he  could  not  write.  Although  he  recovered 
sutficiently  to  return  to  business,  he  continued  to  have  a 
difficulty  about  words  and  the  names  of  persons.  He  also  had 
occasionally  difficulty  in  writing — he  w^ould  write  a  name 
wrong,  know  that  it  was  wrong,  but  could  not  put  it  right. 
His  speech  difficulty  was  also  worse  when  he  felt  tired.  On 
one  occasion  he  had  a  definite  feeling  of  weakness  in  the  left 
arm  and  leg.  I  saw  him  after  he  had  been  carefully  dieted, 
and  had  taken  iodide  of  potassium  for  some  time.  The  radial 
artery  was  thickened  and  felt  segmented,  the  brachial  felt  hard 
and  thick,  and  the  htTemomanometer  gave  a  pressure  of  185 
mm.  Hg.  He  was  well  nourished  with  a  somewhat  florid 
complexion,  was  said  to  be  a  comparatively  spare  eater  and 
temperate  in  his  use  of  liquor.  All  his  life  he  had  suffered 
from  a  "  costive  habit." 

Case  72. — Mrs.  C,  set  68,  was  admitted  to  Queensberry 
House,  and  1  saw  her  on  10th  June  1907.  The  history  was 
that  three  years  ago  she  had  a  fit  and  lost  the  power  of  speech 
and  of  the  right  hand.  She  developed  delusions,  and  was  sent 
to  an  asylum,  but  was  discharged  in  six  months.  Now  and 
again  she  loses  power  in  the  right  arm  and  leg,  but  she  thinks 
she  was  never  so  powerless  as  at  present.  She  says  that  she 
was  walking  about  last  week  with  the  help  of  a  stick,  and  that 
she  lost  power  in  the  end  of  the  week.      The  grasp  of  the 

170 


PERMANENT  PARALYSIS  OR  PARESIS 

right  hand  was  feeble,  there  was  weakness  of  the  right  leg, 
but  she  could  draw  it  up  and  extend  it  as  she  lay  in  bed. 
On  the  left  foot  the  toe  and  ankle  reflexes  were  normal  to 
stroking  the  sole,  on  the  right  foot  there  was  shght  dorsi- 
flexion  of  the  big  toe,  and  no  movement  of  the  other  toes, 
while  the  ankle  reflex  was  active.  The  knee  jerk  was  better 
marked  on  the  left  side  than  on  the  right.  On  13  th  June 
she  had  improved  sufficiently  to  be  able  to  stand ;  the  sole 
reflex  of  the  right  foot  was  again  active;  the  pulse  was  80, 
and  the  hsemomanometer  gave  a  pressure  of  200  mm.  Hg. 

On  29th  June  she  was  again  seized  still  more  seriously 
to  all  appearance.  She  was  dazed  looking  and  speechless, 
and  she  could  not  move  the  right  arm  and  leg.  I  ordered 
half  a  grain  of  erythrol,  which  was  not  repeated,  as  the  patient 
was  in  such  a  state  of  apparent  collapse  that  I  was  afraid  to 
repeat  it.  In  the  evening  she  ralKed,  for  when  the  nurse 
asked  how  she  was  feeling  the  prompt  reply  was  "  fine."  The 
following  morning  when  I  saw  her  she  was  sitting  up  in  bed 
taking  breakfast.  Speech  was  rambling,  but  as  the  day  passed 
she  became  more  sensible.  Power  gradually  returned  on  the 
right  side.  She  had  kept  well  up  to  the  end  of  September, 
when  this  note  was  written.  She  is  a  cheerful,  contented 
woman,  able  to  be  out  of  bed  daily,  and  to  move  about  her 
room.  There  is  no  impairment  of  speech.  She  is  one  of  the 
patients  in  whom  the  radial  artery  suggests  nothing  near  the 
pressure  of  200  obtained  from  the  brachial. 

GEOUP  lY. — FATAL    CASES    OF    HEMIPLEGIA. 

This  group  is  confined  to  fatal  cases  and  in  connec- 
tion with  them  I  seek  to  draw  attention  to  the  tendency 
to  regard  such  cases  as  due  to  cerebral  htemorrhage.  This 
tendency  extends  to  the  kind  of  case  illustrated  in  the 
preceding  group.  The  tendency  to  diagnose  htemorrhage 
seems  to  me  to  have  become  much  more  widespread  amongst 
practitioners  than  it  used  to  be,  and  this  can  only,  I  presume, 
be  attributed  to  their  teachers,  for  the  opportunities  of  check- 
ing diagnoses  are  not  large  in  general  practice.  I  begin  the 
group  with  two  cases  which  may  be  taken  as  typical  of  their 
kind,  and  follow  them  with  other  two  cases  which,  from  their 

171 


CONTRACTION  OF  CEREBRAL  ARTERIES 

clinical  manifestations,  might  have  been  held  to  be  cases  of 
haemorrhage,  did  not  the  post-mortem  examination  confirm  the 
contrary  opinion. 

Two  Fatal  Cases  Illusteatixg  the  Oedinaey  View. 

Case  7  3  was  an  old  gentleman  of  7 1  years  whom  I  saw  in 
consultation.  He  had  been  seized  on  the  morning  of  the  day 
I  saw  him  with  right  hemiplegia  and  aphasia.  This  occurred 
when  he  was  slowly  convalescing  from  what  appeared  to  have 
been  an  attack  of  influenza  with  bronchopneumonia,  so  that 
his  general  condition  was  low  and  his  circulation  poor.  The 
loss  of  power  was  not  accompanied  by  loss  of  consciousness. 
The  pulse  when  I  saw  him  was  soft  and  the  blood-pressure 
low\  There  was  no  albumin  in  the  imne.  The,  patient 
became  worse  in  a  few  days,  and  died  comatose.  The  ordinary 
view  of  such  a  case  would  be  that  it  began  with  a  haemorrhage, 
small  in  size,  but  sufficient  while  destroying  some  fibres  to  press 
upon  adjoining  ones ;  and  that  this  initial  htiemorrhage  was 
followed  by  a  second  and  a  larger  one  in  a  few  days.  There 
was  no  joost-mortcm  examination,  and  so  there  was  no  oppor- 
tunity of  checking  the  ordinary  clinical  opinion  in  this  instance. 
The  symptoms,  however,  closely  resembled  those  in  cases 
in  which  there  was  softening  but  uo  haemorrhage,  as  proved 
by  post-mortem  examination,  and  I  hold  that  these  cases  guide 
us  as  to  the  nature  of  the  lesion  in  such  cases  as  this. 

Case  74  was  a  man  aged  28,  admitted  to  the  Eoyal 
Infirmary  with  left  hemiplegia  without  loss  of  consciousness. 
He  had  been  in  the  Infirmary  some  months  previously,  and 
was  known  to  have  advanced  chronic  kidney  disease.  His 
arteries  were  thick  and  hard.  He  was  markedly  urtemic, 
sometimes  noisy  and  talkative,  at  other  times  semicomatose  or 
drowsy,  but  he  recognised  the  Ward  Sister,  and  could  give  the 
names  of  relations  admitted  to  see  him.  In  three  days  his 
-temperature  suddenly  shot  up  to  105"  to  106°,  he  became 
comatose,  and  died  within  twenty-four  hours.  My  interpreta- 
tion of  the  phenomena  was  that  on  admission  the  blood  supply 
to  the  motor  strand  on  the  right  side  had  been  obstructed, 
and  as  his  vessels  were  markedly  constricted  I  leant  to  the 

172 


FATAL  CASES  OF  HEMIPLEGIA 

view  of  cerebral  vessel  constriction  to  explain  the  arrest. 
The  blood-pressure  was  180''  by  Ohver's  heemomanometer, 
taken  about  twenty  hours  after  treatment  had  been  Ijegun. 
There  was  no  alleviation  of  his  condition  save  that  he  became 
less  noisy.  The  final  coma  with  the  great  rise  in  temperature 
I  attributed  to  haemorrhage.  This  case  in  so  far  as  the  main 
cerebral  symptoms  were  concerned — the  hemiplegia  without 
loss  of  consciousness  ending  in  profound  coma  in  a  few  days 
— closely  corresponded  with  the  main  phenomena  in  Case  73. 
The  post-mortem  examination  here  showed  a  large  fresh  clot 
in  the  usual  region,  involving  the  internal  capsule  and  adjoin- 
ing structures  ;  round  the  clot  there  was  a  distinct  area  of 
softening. 

In  this  case  the  symptoms  on  admission  were  referred  to 
urtemia  and  to  the  arrest  of  blood  supply  to  the  motor  strand 
in  the  right  hemisphere ;  the  later  symptoms  were  referred  to 
haemorrhage.  In  this  case  also  the  ordinary  view  is  that  an 
initial  small  hiemorrhage  is  followed  by  a  second,  larger  and 
fatal  one.  The  paralysis  without  loss  of  consciousness  is, 
however,  satisfactorily  explained  by  a  local  arrest  of  blood 
supply  so  complete  as  to  lead  to  rapid  softening  of  the  portion 
of  brain  affected,  while  the  later  loss  of  consciousness  resulted 
from  haemorrhage  taking  place  into  the  already  softened  area. 
The  appearances  at  the  post-mortem  examination  warrant  this 
contention,  for  the  blood  clot  was  quite  recent,  while  there  was 
a  distinct  zone  of  softened  brain  tissue  round  it.  A  minor 
observation  in  Case  76  gives  support  to  this  contention.  The 
possibility  of  such  a  sequence  of  events  has  not,  so  far  as  I 
know,  been  hitherto  considered,  it  being  assumed  that  such 
cases  were  cases  of  haemorrhage  from  outset  to  finish. 


Two  Fatal  Cases  with  Softening. 

Case  75  was  a  woman,  aged  75,  who  had  been  an 
inmate  for  many  years  of  Queensl^erry  House.  When  I  saw 
her  in  the  forenoon  she  had  paralysis  of  the  left  side  of  the 
face  and  of  the  left  arm,  she  could  draw  the  left  leg  up  a 
little  when  asked  to  do  so.  She  was  conscious.  The  pulse 
was    80,  and   the  blood-pressure  was    135"   to    140^      The 

173 


CONTRACTION  OF  CEREBRAL  ARTERIES 

paralysis  had  come  on  in  the  early  hours  of  the  morning,  and 
had  been  preceded  by  great  restlessness.  The  women  who 
occupied  the  same  room  volunteered  the  information  that  she 
had  been  "  strange  in  her  mind  "  for  a  week  past,  that  she 
"  knew  nothing,"  and  was  "  quite  vacant."  I  saw  her  first  on 
the  11th  of  November,  and  that  afternoon  she  was  put  on 
small  doses  of  erythrol  tetranitrate,  which  were  continued  for 
some  days,  but  was  stopped,  as  there  was  no  diminution  in  the 
degree  of  paralysis.  On  the  17th  her  face  was  flushed,  her 
temperature  was  101°,  and  her  radial  vessels  were  relaxed. 
She  had  slight  bronchitis,  and  during  the  day  her  breathing 
seems  to  have  become  oppressed,  and  she  died  quietly  that 
same  evening.  The  post-mortem  examination  showed  a  sub- 
cortical area  of  softening,  about  the  circumference  of  a  florin, 
in  the  upper  part  of  the  parietal  lobe,  posterior  to  the  ascend- 
ing parietal  convolution,  the  grey  matter  over  it  beiug  a  mere 
film.  There  was  also  distinct  although  moderate  softening, 
involving  the  internal  capsule  on  the  same  side.  There  was 
no  haemorrhage.  The  cerebral  veins  were  engorged,  and 
there  was  a  large  amount  of  fluid  left  in  the  skull  when  the 
brain  was  removed.  The  kidneys  were  atrophied  and 
granular. 

In  this  case  the  possibility  of  a  secondary  htemorrhage 
was  suggested  by  its  presenting  a  certain  resemblance  to  Case 
74  in  the  terminal  phenomenon  of  a  rise  in  temperature,  and  yet 
it  was  found  to  be  one  of  pure  softening,  with  such  a  brain 
oedema  as  is  frequently  found  in  old  people  with  atrophied 
kidneys. 

Case  76. — Peter  M.,  set  74,  was  the  victim  of  a 
harmless  delusion.  On  the  night  of  the  9th  December  1906, 
he  became  restless,  got  out  of  bed,  wandered  about  the  room 
in  which  he  slept,  and  when  I  saw  him  on  the  morning  of  the 
10th  he  was  full  of  delusions.  I  admitted  him  to  my  ward 
in  the  Infirmary  that  same  day.  He  was  kept  in  bed  and 
was  quite  quiet,  but  had  a  fixed  delusion  that  he  had  been 
assaulted.  On  the  morning  of  15  th  December  he  was  found 
by  the  nurse  to  have  lost  the  power  of  the  right  side  and  to 
be  speechless.  When  I  saw  him  at  11.30  a.m.,  he  was  lying 
on  his   back  with  the  eyes  open  and  all  the  appearance  of 

174 


FATAL  CASES  WITH  SOFTENING 

consciousness :  when  spoken  to  he  made  no  reply  and  gave 
no  sign  of  hearing  what  was  said  to  him.  The  face  was  not 
paralysed,  and  when  he  yawned  the  lips  moved  symmetrically. 
The  right  arm  was  not  moved,  while  he  moved  the  left  one 
freely.  The  right  arm  was  somewhat  rigid  at  the  elbow  and 
shoulder ;  the  forearm  was  flexed,  and  was  straightened  with 
some  difficulty.      The  fingers  were  not  rigid.      Sensibility  to 


C.I    "^ 


Fig.  32. — Section  of  brain  from  Case 
76,  showing  three  areas  of  softening, 
a,  h,  c.  In  c  there  was  a  small  recent 
hfemorrhago. 


Fig.  33. — Another  section  of  brain 
from  Case  76,  showing  area  of  softening 
at  b.  ,  Dr.  Carnegie  Dickson  kindly 
made  the  tracings  from  which  these 
photographs  were  taken. 


pinching  was  absent  or  much  diminished  in  the  right  arm, 
but  present  in  the  left.  He  did  not  move  the  legs,  but  when 
they  were  passively  drawn  up  they  remained  in  that  position. 
When  pinched  he  drew  them  up  a  little.  The  response  to 
tickling  the  soles  was  very  active  on  the  left  side,  but  absent 
on  the  right.  There  was  no  ankle  clonus.  Both  knee  jerks 
were  active.  He  had  passed  urine  and  fteces  in  bed.  There 
was  no  albumin.      The  pulse  was  between  70   and   80  and 

175 


CONTRACTION  OF  CEREBRAL  ARTERIES 

slightly  irregular,  the  vessel  wall  was  thick,  the  haemomanometer 
registered  from  180°- 190°.  He  was  put  on  erythrol  tetra- 
nitrate,  and  on  the  20th  iodide  of  potassium  was  also  given. 
No  marked  change  occurred  in  the  symptoms ;  on  the  21st  it 
was  noted  that  he  gave  his  left  hand  slowly  when  asked  to 
shake  hands.  The  patient  died  on  the  27th  of  acute  pleurisy, 
with  some  patches  of  broncho-pneumonia  in  the  lobe  affected 
with  the  pleurisy.  The  brain  on  the  left  side  showed  two 
considerable  areas  of  subcortical  softening,  into  one  of  which 
there  was  a  small  recent  hasmorrhage ;  and  a  considerable 
area  of  softening  into,  and  in  the  neighbourhood  of,  the  lenti- 
cular nucleus. 

In  this  patient  death  was  the  result  of  a  definite  inter- 
current acute  disease,  so  that  the  opportunity  was  afforded  of 
checking  the  diagnosis  of  cerebral  softening. 

Sections  of  the  brain  at  two  different  levels  are  shown  in 
the  accompanying  figures.  The  softened  areas  are  shaded. 
In  the  posterior  area  marked  c  there  was  a  recent  haemorrhage 
about  the  size  of  a  hazel  nut.  This  had  undoubtedly  taken 
place  into  an  area  already  softened,  and  tends  to  strengthen 
my  opinion  that  fatal  hsemorrhages  may  not  infrequently  be 
due  to  a  primary  softening,  so  that  even  post-mortem  appear- 
ances may  be  quite  misleading  unless  the  possibility 
mentioned   is    fully   recognised. 

GROUP   V. — TWO    SPECIAL   CASES. 

Case  77. — Temporary  paresis  acooynpanying  paroxysms  of 
angina  2^ectoris. — In  this  patient,  Mrs.  M.,  £et.  49,  the 
leading  feature  was  the  recurrence  at  intervals  of  about  four 
weeks  of  symptoms  typical  of  angina  pectoris,  while  the  most 
striking  phenomenon  was  the  association  of  left  hemiparesis 
with  them.  She  had  her  first  attack  of  angina  pectoris  seven 
years  before  I  saw  her.  During  that  attack  the  left  arm  was 
paralysed,  but  it  regained  the  greater  part  of  the  lost  power 
in  twenty-four  hours ;  still,  she  asserts  that  it  has  never  been 
as  strong  as  the  other  one  since  then.  The  history  given  to 
me  by  her  medical  attendant.  Dr.  Blackstock  of  Eskbank, 
was  that  every  few  weeks  she  suffered  from  angina  pectoris ; 
that  when  this  supervened  she  became  hemiplegic ;  and  that 

176 


TWO  SPECIAL  CASES 

when  the  anginous  attacks  were  cured  the  hemiplegia  passed  off. 
This  corresponded  with  the  history  I  gathered  by  questioning 
the  patient  myself ;  but  I  further  ascertained  from  her  that 
even  when  moving  about  the  house,  if  she  took  an  anginous 
attack,  her  left  arm  became  affected,  and  that  she  had  often 
lost  the  use  of  the  arm  for  from  twenty  minutes  to  an  hour. 
During  the  two  occasions  she  was  under  my  care  in  the 
Infirmary  she  had  slight  weakness  of  the  left  arm  and  leg, 
and  there  was  also  a  partial  or  complete  loss  of  tactile 
sensibility  in  these  limbs.  It  is  not  necessary  to  record  here 
all  the  details  of  this  case,  for  the  important  facts  are  those 
I  have  given,  and  it  is  their  interpretation  which  specially 
concerns  me  at  present.  I  was  fortunate  enough  to  see  this 
patient  in  a  slight  anginous  attack,  and  in  it  there  was  the 
usual  hypertonic  contraction  of  her  arteries.  The  recurring 
and  close  association  of  the  anginous  attacks  with  recurring 
hemiplegia  or  brachial  monoplegia  had  been  so  frequently 
noted,  that  it  seemed  to  me  there  was  no  possible  explanation 
of  the  association  but  by  regarding  the  abeyance  of  motor 
power  to  be  due  to  a  temporary  lessening  or  cutting  off  of 
the  blood  supply  to  the  motor  strand  in  the  brain,  the  result 
of  a  spasm  contraction  of  cerebral  vessels ;  the  cerebral  vessel 
spasm  accompanying  the  systemic  vessel  spasm  of  the 
anginous  attack.  In  this  case  changes  of  the  kind  mentioned 
seem  to  me  a  necessity  for  the  explanation  of  the  clinical 
phenomena,  and  it  would  be  most  unfortunate  if  physiologists 
regarded  such  phenomena  as  having  no  bearing  upon  their 
special  department  of  investigation.  Measures  directed  to  the 
improvement  of  the  general  vascular  condition  led  to  very 
satisfactory  results. 

Case  78. — Old-standing  right  hemiparesis  loith  temporary 
attack  of  comp)lete  rigid  hemiplegia  and  aphasia.— This  case, 
a  man  of  58  years,  was  a  partial  recovery  from  an  old 
hemiplegia.  He  was  able  to  walk  about  and  look  after 
himself  in  spite  of  a  disabled  right  arm  and  leg.  His  speech 
was  somewhat  mumbling,  although  he  could  speak  so  as  to  be 
understood.  I  saw  him  one  morning  soon  after  he  had  so 
completely  lost  power  in  his  disabled  limbs  that  he  could  not 
move  them,  while  he  had  so  entirely  lost  the  power  of  speech 
M  177 


CONTRACTION  OF  CEREBRAL  ARTERIES 

that  he  could  not  utter  an  articulate  sound.  He  was  quite 
conscious,  and  evidently  greatly  annoyed  at  his  inability  to 
speak,  or  to  get  out  of  bed.  His  vessels  were  thick  and 
contracted,  and  measures  w^ere  at  once  taken  for  their  relaxa- 
tion. He  had  considerably  improved  by  the  following  day, 
and  two  days  later  he  had  regained  his  former  power  both  of 
locomotion  and  of  speech.  That  the  symptoms  here  were 
due  to  an  interference  with  the  blood  supply  of  the  damaged 
area  in  his  brain  is,  I  think,  beyond  question ;  that  he  would 
not  so  speedily  have  recovered  had  the  condition  been  local 
thrombosis  is  equally  beyond  question ;  w^hile  the  occurrence 
of  vessel  constriction  readily  explains  the  loss  of  power — the 
prompt  relaxation  explaining  the  speedy  recovery. 

GROUP  VI. — CHEYNE-STOKES   BREATHING  WITH  THICK 

ARTERIES. 

This  case  is  interesting,  and,  taken  along  with  the  other 
observations  in  this  chapter,  is  instructive,  although  mean- 
while it  stands  by  itself. 

Case  79. — E.  K.,  a  man  aged  70,  had  been  for  a  short  time 
in  Queensberry  House.  It  is  unnecessary  to  dwell  upon  his 
condition  before  he  came  under  particular  observation.  In  the 
middle  of  May  1 9  0  7  he  was  confined  to  bed  with,  it  was  stated, 
difficulty  of  breathing.  He  was  given  spirit  of  nitrous  ether  and 
stramonium  tincture.  For  some  days  his  condition  was  very 
critical,  so  bad  that  the  nurse  had  been  summoned  several  times 
as  it  was  thought  he  was  dead.  I  saw  him  on  the  28  th  May, 
when  he  was  said  to  have  somewhat  improved.  His  condition 
was,  however,  still  serious :  he  had  marked  Cheyne-Stokes 
breathing,  the  period  of  apnoea  lasting  for  thirty-five  seconds, 
the  period  of  breathing  for  thirty  seconds.  This  rhythm  was 
quite  regular  durmg  the  times  I  saw  him.  The  pulse  varied 
from  48  to  120  per  minute,  being  very  irregular  both 
in  force  and  time.  On  the  29  th  his  pressure  was  about 
200  mm.  Hg.,  the  radial  artery  was  much  thickened  and 
hard.  The  heart  dulness  was  in  the  nipple  line,  there  were  no 
murmurs  ;  there  was  no  albumin  in  the  urine.  The  breathing 
continued  the  same  as  on  the  previous  dav.      The  pulse  was 

178 


CHEYNE-STOKES  BREATHING 

very  irregular,  there  being  a  large  beat  followed  by  a  varying 
number  of  small  beats,  as  shown  in  the  tracing  (Fig.  34). 


r^  t 


S       *C 
■■::      to 


S   2 


^-2 


cr  o 


179 


CONTRACTION  OF  CEREBRAL  ARTERIES 

The  observations  by  the  hfemomanometer  were  specially 
instructive.  I  was  using  the  wrist-pad  to  determine  when 
the  brachial  artery  became  occluded,  and  I  noted  that  with  the 
pressure  at  180  all  the  pulse  waves  were  present  in  the  radial ; 
at  190  only  the  large  waves  seen  in  the  tracing  were  present  in 
the  radial ;  while  at  200  all  waves  were  stopped.  I  put  him  on 
half  a  grain  of  erythrol  tetranitrate  four  times  in  twenty-four 
hours  and  a  mixture  containing  squill  and  iodide  of  potassium 
to  be  taken  thrice  daily.  On  May  31st  I  took  the  tracmg 
(Fig.  35),  the  first  half  being  taken  during  a  period  of  ai^noea, 
the  second  during  a  period  of  deep  breathing.  After  a  few 
days  of  this  treatment  great  improvement  was  apparent. 
The  Cheyne-Stokes  breathing  steadily  lost  its  special  character, 
he  slept  soundly  during  the  night,  and  the  pulse  became  much 
more  re^ndar.      On  June  9th  the  dose  of  ervthrol  was  reduced 


Fig.  36. — Tracing  from  Case  79,  taken  on  26th  June  when  patient  had 
recovered  ;  hseniomanonieter  pressure,  200  mm.  Hg. 

to  ^  grain  four  times  in  twenty-four  hours  ;  and  on  June  10th 
it  was  stopped.  The  pulse  was  much  more  regular  in  force, 
and  beat  about  70  per  minute.  Notwithstanding  the  re- 
markable degree  of  improvement  in  this  patient's  condition, 
due  undoubtedly  to  the  erythrol,  at  no  time  did  I  get  his 
pressure  below  200  mm.  Hg. :  and  yet  that  his  capillary 
circulation  was  relaxed  was  seen  by  the  rosy  tint  of  his  face 
and  lips,  and  that  the  radial  was  somewhat  softened  was  felt 
by  the  finger.  I  take  it  that  the  brachial  was  not  appreciably 
influenced,  and  so  the  manometer  reading  remained  much 
the  same  as  before.  On  the  26th  June  I  took  the  above 
tracing  Fig.  36  from  the  radial  artery.  It  shows  the  great 
improvement  that  took  place  in  the  pulse,  representing,  of 
course,  a  like  improvement  in  the  heart.  The  Cheyne- 
Stokes  breathing  had  absolutely  disappeared  long  before  this. 
The  case  was  of  varied  interest,  and  I  am  not  sure  that  I 

i8o 


CLINICAL  PATHOLOGY  OF  PRECEDING  GROUPS 

ever  saw  so  severe  a  case  recover.  The  haemomanometer 
observations  were  of  special  interest,  as  thej  so  clearly  showed 
that  a  rise  of  less  than  10  mm.  Hg.  above  180°  prevented 
the  smaller  waves,  shown  in  the  sphygmographic  tracing, 
reaching  the  wrist;  while  a  rise  of  less  than  10  mm.  more 
obliterated  the  large  waves  also. 

Since  the  foreo-oino-  was  written  this  man  has  had 
another  seizure,  but  as  soon  as  the  symptoms  appeared  he 
was  put  on  erythrol  every  four  hours,  and  on  iodide  of 
potassium  and  squill  thrice  daily.  He  was  kept  exclusively 
on  milk.  He  made  a  speedy  recovery,  and  was  able  to  be 
out  of  bed  and  to  move  about  within  a  fortnight.  The 
second  attack  was  undf)uljtedly  induced  by  the  attentions  of 
his  friends  in  supplying  a  variety  of  additions  to  his  ordinary 
plain  dietary. 

THE   CLIXICAL   PATHOLOGY    OF    THE    PRECEDING 
GROUPS    OF    CASES. 

Transitory  and  recurring  Phenomena. — It  is  un- 
necessary to  multiply  such  cases,  for  if  those  given  cannot 
be  made  the  basis  of  a  convincing  argument,  a  larger  number 
would  not  carry  conviction. 

The  cases  I  have  given  seem  to  me  to  constitute  a  series 
of  phenomena  which  are  so  linked  as  to  form  an  unbroken 
chain ;  and  which  can  only  be  satisfactorily  explained  and 
linked  on  the  grounds  which  can  now  be  indicated. 

Minor  Phenomena  and  Focal  Spasm.^ — Beginning  with 
the  minor  manifestations,  such  as  those  in  Group  I.,  I  believe 
they  are  all  explicable  on  the  assumption  that  they  were  due 
to  anmmia  of  brain  areas,  that  the  local  ancemia  was  due  to 
hypertonic  contraction  or  to  spasm  constriction  of  the  vessels  in 
those  areas.  The  spasm  of  cerebral  vessels  may  have  been  an 
accompaniment  of  a  general  hypertonic  contraction,  and  in 
some  cases  it  undoubtedly  was ;  that  general  contraction  is 
a  necessary  accompaniment  is  by  no  means  certain.  The 
fact  that  local  or  limited  arterial  spasm  has  been  recognised 
in  migraine  has  l3een  already  referred  to,  also  tlie  fact  that 
temporary  local  paralyses  are  known  to  accompany  the 
migrainous  attack.       It  seems  to  me  that  local  spasm-con- 

i8i 


CONTRACTION  OF  CEREBRAL  ARTERIES 

striction  of  cerebral  arteries  is  made  clinically  certain  by  these 
observations.  But  this  hypothesis  can  be  supported  by  other 
clinical  facts.  I  know  a  medical  man  who  could  not  drink 
beer  because  it  gave  him  migraine ;  and  he  had  further 
observed  that  the  temporal  artery  on  the  side  of  the  migraine 
was  hard  and  thick  during  the  attack.  Another  medical 
man  informed  me  that  as  a  student  he  discovered  that  if  he 
had  poached  eggs  to  breakfast  he  had  an  attack  of  migraine 
as  a  consequence.  This  same  medical  man  told  me  that  with 
him  a  migraine  w^as  usually  accompanied  by  a  certain 
difficulty  in  getting  the  right  word.  Without  going  further 
afield  for  evidence  of  the  same  kind,  I  hold  that  in  such 
phenomena  we  have  clear  clinical  proof  that  some  substances 
(in  one  case  a  simple  dietetic  substance,  in  another  what  can 
ordinarily  be  regarded  as  a  harmless  beverage)  act  on  certain 
persons  as  poisons,  and  confine  their  action  to  certain  nervous 
areas,  acting  presumably  on  the  blood  vessels  of  tlie  particular 
area  affected.  Very  strong  support  is  given  to  this  view  by 
the  ocular  phenomena  which  have  been  noted  in  severe  cases 
of  quinine  poisoning.  Again  I  am  indebted  to  Mr.  E. 
Marcus  Gunu  for  information.  He  kindly  sent  me  the 
following  memorandum  : — -In  severe  cases  of  quinine  poisoning 
the  ocular  symptoms  are  usually  complete  or  partial  blind- 
ness, associated  with  marked  narrowing  of  the  retinal  arteries 
and  pallor  of  the  optic  discs.  Sometimes  at  first  the 
ophthalmoscopic  appearances  resemble  those  present  in 
embolism,  or  thrombosis,  of  the  central  artery.  As  a  rule 
recovery  takes  place,  but  this  is  often  much  delayed.  It  is 
said  that  a  second  attack  may  be  the  result  of  a  comparatively 
small  dose.  Pathologically,  in  lower  animals,  no  changes 
have  been  found  in  the  vessels  during  the  first  month  or  so, 
although  they  are  ophthalmoscopically  small.  After  two 
months,  the  arteries  have  been  found  to  have  thickened  walls 
with  contracted  lumen. 

Here,  then,  is  a  substance  having,  as  part  of  its  poisonous 
effect,  a  marked  localised  effect  on  the  arteries,  causing  their 
constriction,  and  ultimately  leading  to  the  thickening  of  their 
walls  and  diminution  in  their  lumen.  It  is  difficult  to  see 
how  we  are  to  get  evidence  more  conclusive  than  this. 
The  vessels  inside   the   brain  can  never  be  watched  as  the 

182 


CLINICAL  PATHOLOGY  OF  PRECEDIXG  GROUPS 

retinal  vessels  can  be  watched  ;  Ijiit  I  hold  that  my  series  of  cases 
requires  a  similar  clinical  pathologj  for  their  interpretation, 
and  few  will  hesitate  to  accept  the  interpretation  as  a  valuable 
and  practical  working  hypothesis  in  corresponding  cases. 

The  Special  Irritant. — The  question  of  the  special  irritant, 
when  there  is  merely  focal  vessel  spasm  in  a  brain  region, 
can  only,  so  far,  be  a  matter  of  surmise.  Still,  even  surmise 
may  have  a  practically  useful  side.  My  hypothesis  is  that 
the  spasm  in  such  cases  is  caused  by  local  fatigue  products, 
or  by  waste  products,  so  irritating  the  vessels  as  to  cause 
their  constriction.  The  effect  of  such  products  seems  to  me 
always  to  be  of  this  nature.  Experimentally  it  is  known  that 
fatigue  products  accumulating  in  muscle  prevent  its  response 
to  electrical  stimulation.  These  products  can  be  artificially 
washed  out,  after  which  the  response  to  stimulation  returns. 
It  is,  further,  a  well-known  fact  that  hot  bathing  is  one  of  the 
best  means  of  recovering  from  a  sense  of  fatigue.  The  action 
of  the  hot  bath  is  so  to  dilate  the  vessels  that  the  flow 
through  them  is  facihtated  and  the  fatigue  products  are  more 
promptly  removed.  In  migraine  whatever  relaxes  the  vessels 
cures  the  symptoms. 

The  Phenomena  in  Persons  with  Sclerosed  Vessels.— 
There  is  another  aspect  of  some  of  the  cases  with  recurring  cere- 
bral phenomena  which  has  to  be  dealt  with.  In  persons  with 
sclerosed  or  atheromatous  arteries,  my  experience  is  that  the 
cerebral  phenomena  are  associated  with  hypertonic  contraction 
of  systemic  vessels.  I  presume  that  in  these  cases  the 
same  cause  which  excites  contraction  of  systemic  vessels  is 
operating  on  the  cerebral  vessels — that,  in  fact,  there  are 
substances  in  the  blood  which  are  acting  directly  on  both, 
and  are  therefore  not  acting  through  the  vasomotor  centre. 
Of  this  association  I  am  fully  satisfied ;  the  only  point 
which  appears  to  me  to  be  open  to  question  is  whether  this 
association  is  usually  present  in  persons  with  normal  vessels. 
My  own  experience  does  not  allow  me  to  form  an  opinion  on 
this  point.  When  hypertonic  contraction  is  present  in  the 
systemic  vessels,  it  gives  great  confidence  in  adopting  the 
appropriate  treatment,  while  the  hsemomanometer  provides, 
as  a  nde,  a  valuable  record  of  the  effect  treatment  is 
exercising  on  the  vessels. 

183 


CONTRACTION  OF  CEREBRAL  ARTERIES 

When,  along  with  systemic  hypertonic  contraction,  there 
is  paralysis,  it  can  be  accounted  for  by  the  vessels  in  the 
particular  area  of  brain  affected  having  undergone  greater 
structural  alterations  than  elsewhere.  This,  however,  leads 
now  to  the  consideration  of  the  cases  of  temporary  and  per- 
manent paralysis  in  persons  whose  arteries  are  thickened. 

Temporary  and  Permanent  Paralysis  in  Persons  with 
Sclerosed  Vessels. 

In  Cases  6  8  and  771  have  shown  how  unreasonable,  and  even 
absurd,  it  would  be  to  regard  the  recurring  paretic  phenomena 
as  due  either  to  haemorrhage  or  to  thrombosis.  That  multiple 
attacks  of  temporary  paralysis  could  be  caused  by  an  equally 
numerous  number  of  hasmorrhages  is  quite  unthinkable,  and 
this  is  also  the  position  as  regards  thrombosis.  The  only 
explanation  possible  is  to  regard  the  paretic  attacks  as  due 
to  recurring  partial  arrest  of  the  blood  supply  to  the  motor 
strand,  and  the  only  conceivable  way  in  which  this  could  be 
brought  about  is  by  vessel  constriction.  The  systemic  vessels 
showed  this  constriction,  while  cerebral  vessel  constriction 
occurring  coincidently  would  explain  the  paretic  phenomena. 

In  Case  78  the  rapid  recovery  from  the  total  paralysis 
seems  to  me  to  exclude  the  idea  of  either  haemorrhage  or 
thrombosis  having  occurred  in  the  already  damaged  motor 
strand  in  the  brain.  Either  of  these  in  such  a  damaged  area 
would  have  inevitably  led  to  a  permanent  loss  of  power,  and 
yet  no  such  loss  resulted.  I  know  of  no  other  way  to  account 
for  the  temporary  lowering  of  the  circulation  in  the  damaged 
area  than  by  assuming  that  vessel  constriction  had  occurred. 

Looking  further  at  Case  68,  I  again  contend  that  it  is 
most  unreasonable  to  suppose  that  there  was  even  a  small 
haemorrhage  into  the  brain.  A  small  haemorrhage  into  the 
motor  strand  would  destroy  some  fibres  permanently,  a  fact 
equally  true  of  thrombosis,  unless  the  collateral  circulation 
were  very  promptly  established,  which  in  the  brain  cannot  be 
assumed  as  likely.  The  pronounced  motor  paralysis  with 
aphasia  must  have  been  due  to  a  partial  arrest  in  the  blood 
supply  to  the  great  motor  strand ;  the  arrest  cannot  have 
been  complete,  for  had  it  l^een,  softening  would  have  taken 

184 


TEMPORARY  AND  PERMANENT  PARALYSIS 

place  rapidly,  with  a  destruction  of  fibres  from  which  there 
would  have  been  no  complete  recovery.  Here  again  the  only 
satisfactory  explanation  of  the  complete  restoration  is  found 
in  assuming  that  there  was  cerebral  vessel  constriction 
diminishing  blood  supply  for  the  time,  but  passing  off,  and 
again  permitting  the  normal  nutrition  of  the  affected,  area. 
In  this  particular  case  tlie  paralysis  was  preceded  by  a 
period  of  restlessness  and  mild  delirium ;  such  an  upset  of 
brain  function  as  is  to  be  attributed  to  a  disturbance  of 
cerebral  circulation.  The  sequence  of  phenomena  is  fairly 
common  in  old  people,  and  is  noted  in  Case  76  also,  and  is 
an  argument  in  support  of  my  view  that  the  paretic 
phenomena  result  from  transitory  vessel  changes  just  as  the 
mental  phenomena  do.  Had  the  focal  aneemia  persisted  or 
been  complete,  softening  would  assuredly  have  followed,  from 
which  there  is  no  restoration.  In  this  case  treatment  by  a 
powerful  vaso-dilator  was  early  adopted,  and,  as  has  been 
seen,  there  was  rapid  recovery  on  three  different  occasions. 
The  result  can  hardly  have  been  mere  coincidence,  that  is 
to  say,  that  the  x^atient  would  have  recovered  as  rapidly  had 
no  such  drug  been  used. 

In  Case  65  such  marked  improvement  followed  when 
treatment  produced  freedom  in  the  capillary  circulation,  that 
it  led  one  to  attribute  the  improvement  in  the  paretic 
phenomena  to  a  like  flushing  of  cerebral  vessels. 

In  Cases  75  and  76  the  softening  in  the  internal  capsule 
or  its  neighbourhood  was  so  much  less  complete  than  in  the 
cortical  softened  areas,  that  the  possibility  of  the  difference 
being  the  result  of  the  administration  of  the  same  drug 
suggested  itself.  If  any  value  is  to  be  attached  to  the 
observations  they  would,  of  course,  support  the  view  of  vessel 
constriction. 

Cerebral  vessel  constriction,  if  it  leads  to  complete  arrest 
of  blood  supply  to  any  portion  of  brain,  will  inevitably  lead 
to  softening  of  the  area  so  deprived  of  nutriment.  This 
diminution  of  blood  supply  to  a  local  area  may  be  due  to 
spasm  constriction  of  the  vessels  in  the  particular  area ;  but 
it  may  also  be  explained  in  another  way.  If  constriction  of 
all  the  cerebral  vessels  occurred  at  the  same  time,  those  areas 
would    suffer    most    where    the    lumen  of    vessels    was   per- 

185 


CONTRACTION  OF  CEREBRAL  ARTERIES 

manently  diminished  by  arteriosclerosis,  by  atheroma,  or  by 
obliterating  endarteritis.  These  changes  frequently  assume 
such  proportions  that  a  general  vessel  constriction  in  the  brain 
would  deprive  the  areas,  where  vessels  were  so  affected, 
entirely  of  their  l^lood  supply,  and  this  would  inevitably  lead 
to  softening.  The  three  pathological  changes  mentioned  cause 
diminution  of  lumen,  and  any  general  constriction  of  brain 
vessels  would  markedly  diminish,  and  might  even  completely 
arrest  the  ckculation  through  the  vessels  so  altered.  In 
addition  to  this,  the  result  in  some  of  the  vessels  would 
certainly  be  thrombosis,  leading  to  permanent  cutting  off  of 
blood  supply  and  inevitable  softening.  The  possibility  of 
vessel  spasm-contraction  leading  to  thrombosis  in  sclerosed- 
vessels,  or  in  the  atheromatous  parts  of  constricted  vessels, 
is  a  new  view,  and  yet  it  naturally  suggests  itself  when 
constriction  is  pictured  as  occurring  in  vessels  which  have 
undergone  the  permanent  anatomical  changes  mentioned. 
Realising  this,  the  occurrence  of  softening,  even  after  relaxa- 
tion has  been  induced,  is  readily  explained,  on  the  reasonable 
assumption  that  constriction  had  lasted  long  enough  to  permit 
of  thrombosis.  It  is  not  necessary  to  argue  that  the  con- 
ditions formulated  are  favourable  to  thrombosis  occurring, 
for  they  correspond  to  those  generally  recognised  as 
sufficient  to  produce  that  condition. 

Softening  or  Haemorrhage  ? 

A  further  point  to  be  considered  is  the  relationship 
between  softening  and  hemorrhage,  this  being  the  ques- 
tion raised  hj  the  phenomena  in  Cases  73  and  74.  In 
Case  74  we  have  both  clinical  history  and  post-mortem 
examination  to  help  us  to  a  conclusion.  When  this  patient 
was  admitted  to  hospital  the  mental  unrest  and  delirium  was 
urtemic  in  origin,  but  was  not  intense  enough  to  prevent  the 
patient  recognising  people  and  answering  questions  when 
directly  spoken  to — he  was  not  unconscious,  and  yet  he  was 
hemiplegic.  Active  measures  were  used  for  the  alleviation 
of  the  ura?mia,  the  reduction  of  blood-pressure,  and  the 
relaxation  of  his  vessels,  the  result  being  that  he  became 
quieter.       In    the    course    of    three    clays    the     temperature 

1 86 


SYMPTOMS  DUE  TO  A  FEEBLE  CIRCULATION 

abruptly  rose,  and  the  patient  became  comatose,  and  died 
with  symptoms  of  general  brain  compression.  The  ordinary  ex- 
planation in  such  cases  is  that  the  hemiplegia  without  loss  of 
consciousness  is  due  to  a  small  haemorrhage,  while  the  later 
coma  is  due  to  a  second  and  larger  bleeding.  Chronic  kidney 
disease  with  marked  vessel  changes,  and  high  blood-pressure 
are  common  precursors  of  such  cerebral  phenomena,  and  are 
commonly  regarded  as  sufficient  to  establish  the  diagnosis  of 
htemorrhage.  There  is,  however,  another  explanation  which 
to  my  mind  is  more  satisfactory-  in  my  case.  It  is  this, 
namely,  that  the  hemiplegia  without  loss  of  consciousness 
was  due  to  a  focal  antemia  determined  l)y  vessel  constriction, 
and  this  led  to  thrombosis,  followed  by  softening.  Into 
this  softened  region  hsemorrhage  occurred  in  about  three 
days,  and  of  this  the  patient  died.  There  is  no  doubt  that 
the  htemorrhage  was  a  terminal  occurrence  in  this  case,  while 
the  fact  that  it  showed  a  zone  of  definite  brain  softening 
round  it  suggests  the  interpretation  that  the  htemorrhage 
occurred  in  what  was  primarily  an  area  of  softening.  I  am 
aware  that  softening  around  a  haemorrhage  may  be  secondary, 
but  the  haemorrhage  in  this  case  was  too  recent  to  have  led 
to  the  softening.  The  facts  in  this  case,  and  the  sequence 
in  which  I  place  them  might  be  accepted  as  also  applicable 
to  Case  73,  where  there  was  no  post-mortem  examination, 
were  it  not  that  Case  7  5  showed  a  somewhat  similar  sequence 
of  clinical  phenomena,  and  yet  there  was  no  htemorrhage, 
only  softening,  to  explain  the  hemiplegia ;  while  the  final 
condition,  instead  of  being  due  to  htemorrhage,  was  due  to 
venous  engorgement  and  brain  oedema,  a  common  sequence  in 
old  people  who  become  comatose  and  have  atrophied  kidneys 
with  weak  hearts. 


Symptoms  due  to  a  Feeble  Circulation. 

The  cerebral  manifestations  dealt  with  cannot  be  left  with- 
out referring  to  another  aspect  of  their  clinical  pathology.  It 
is  a  not  uncommon  experience  to  see  cases  where  the  patient 
has  found  himself  t©  Ije  paralysed  on  awaking  from  sleep  ;  or  the 
nurse  or  a  relative  makes  the  discovery.  The  clinical  pathology 
of  such  cases  is,  I  believe,  as  follows, — during  sleep  cardiac 

187 


CONTRACTION  OF  CEREBRAL  ARTERIES 

action  is  at  its  feeblest  and  the  cerebral  vessels  are  contracted. 
If  the  heart  at  its  best  be  feeble,  and  if  the  cerebral  vessels 
are  sclerosed  or  atheromatous,  the  conditions  during  sleep 
are  just  those  which  would  favour  a  focal  ansemia  which 
might  be  complete  enough  to  lead  to  softening.  That  the 
motor  tract  suffers  so  commonly  is,  I  imagine,  due  to  its 
functional  activity  and  to  its  vessels  being  most  altered.  In 
two  of  my  cases  the  first  areas  softened  were  cortical  areas, 
followed  by  softening  in  the  great  motor  tract.  These  cases 
are  of  great  importance  from  the  standpoint  of  prevention,  for 
I  have  seen  cases  where  it  appeared  to  me  that  fatal  results 
have  followed  upon  a  vigorously  applied  reducing  line  of 
treatment. 

Treatment. 

The  practical  value  of  the  foregoing  contentions  is  that 
they  explain  and  link  together  a  great  number  and  variety  of 
clinical  phenomena,  the  nature  of  which  has  been  obscure ; 
and  that  they  provide  a  new  point  of  view  from  which  treat- 
ment can  be  considered.  The  autonomy  of  the  cerebral 
circulation  no  doubt  introduces  a  factor  which  theoretically 
presents  a  difficulty,  for  it  has  to  be  assumed  that  the 
condition  of  the  systemic  may  not  represent  that  of  the 
cerebral  circulation.  In  this  connection,  however,  the  fact 
that  the  condition  or  composition  of  the  blood  affects  the 
measure  of  vessel  contraction  or  tone  has  to  be  given  a  more 
prominent  place  than  it  has  hitherto  been  accorded.  I  have 
submitted  a  number  of  clinical  observations  to  show  that 
cerebral  symptoms  coincided  with  systemic  vessel  constriction, 
and  that  the  former  disappeared  when  systemic  relaxation 
was  induced.  At  the  same  time,  when  the  autonomous  aspect 
of  the  cerebral  circulation  is  regarded,  it  has  to  be  acknow- 
ledged that  it  would  probably  be  of  much  therapeutic  value 
to  have  more  experimental  data  than  we  possess.  Meanwhile 
we  have  to  be  content  with  such  facts  as  I  have  indicated 
in  the  earlier  part  of  this  chapter,  adding,  however,  to 
these  the  results  of  clinical  experience  with  the  therapeutic 
measures  we  have  at  our  disposal. 

Of    the    considerable    array     of     vaso-dilators     the     one 

i88 


TREATMENT 

which  usually  acts  most  definitely  and  whose  action  can  be 
most  readily  maintained  is  erythrol  tetranitrate.  The  use 
of  this  powerful  dilator  has,  however,  often  to  be  supported 
by  the  administration  of  digitalis,  squill,  or  strophanthus. 
This  is  necessary  when  the  condition  of  the  heart  is  unsatis- 
factory as  regards  strength.  The  estimate  of  the  blood- 
pressure  within  the  constricted  vessels  becomes  thus  of 
first-rate  importance.  For  instance,  if  a  case  of  focal  anaemia 
be  mistaken  for  a  haemorrhage  and  reducing  measures  used,  as 
is  not  uncommon,  these  may  only  slightly  relax  vessels,  while, 
if  the  heart  be  feeble,  they  lower  blood-pressure  so  much  that 
complete  focal  bloodlessness  may  be  induced  with  its  irreparable 
softening  and  possibly  a  secondary  haemorrhage.  If  the  con- 
striction has  already  led  to  thrombosis,  even  prompt  relaxation 
will  not  prevent  a  measure  of  softening  with  its  corresponding 
permanent  disablement.  This  cannot  be  always  avoided,  but 
the  line  of  treatment  indicated  promises  success  in  a  con- 
siderable proportion  of  cases.  Among  the  dilators  which 
I  have  used  may  be  mentioned  spirit  of  nitrous  ether,  iodide 
of  potassium,  belladonna  and  its  alkaloid  atropine,  stramonium, 
valerian,  phenacetin,  trional,  paraldehyde,  or  combinations  of 
these.  There  seems  to  me  to  be  no  doubt  that  when  the 
circulation  is  looked  at  from  the  standpoint  I  have  indicated, 
much  can  be  done  to  prevent  the  occurrence  of  the  changes 
referred  to.  When  the  systemic  circulation  as  judged  of  by 
the  finger  and  the  haemomanometer  shows  a  ready  response 
to  treatment,  the  outlook  is  very  favourable ;  but  when 
cerebral  symptoms  occur  without  corresponding  indications 
in  the  systemic  system,  the  particular  measures  to  be  adopted 
are  determined  by  the  general  estimate  formed  of  the  patient's 
vessels  and  heart.  Measures  can  be  directed  to  allaying  the 
-contractile  irritabihty  of  the  cerebral  vessels  while  maintaining 
as  large  a  volume  of  blood  from  the  heart  as  possible.  In  no 
other  department  of  practical  medicine  can  so  much  be  done 
for  the  prolongation  of  life,  sometimes  of  great  public  value, 
and  for  the  protecting  of  people  from  the  sadness  or  misery 
of  partial  cerebral  disablement,  as  can  be  accomplished  in 
such  cases  by  a  right  understanding  of  circulatory  phenomena  ; 
and  I  am  convinced  that  this  understanding  has  at  its  founda- 
tion the  recognition  of  hypertonic  contraction  of  vessels ;  and 

189 


CONTRACTION  OF  CEREBRAL  ARTERIES 

the  separation  of  this  condition  from  what  is  called  blood- 
pressure.  The  hypertonus  may  be  present  when  the  heemo- 
manometer  registers  115°,  and  it  may  be  absent  when  it 
reo-isters  200".  Sclerosed  vessels  and  atheromatous  vessels 
as  such  are  not  incompatible  with  long  life,  but  as  soon  as 
the  factor  of  hypertonic  contraction  comes  in  there  is  danger. 
Here,  as  in  angina  pectoris,  the  sensitiveness  of  the  vessels 
can  be  reduced  by  rigidly  regulating  the  diet  on  the  lines  I 
have  already  frequently  indicated. 

EEFEREIs^CES. 

W.  Russell,  Brit.  Med.  Journ.,  February  10,  1906  ;  Traits.  Kdin. 
Med.-Chir.  Soc,  1901  ;  Laiicet,  London,  June  1,  1901  ;  Brit.  Med. 
Journ.,  June  A,  1904;  Praditioner,  London,  1906.  H.  G.  Lang- 
•\vill,  Scot.  Med.  and  Surg.  Journ.,  June,  1906.  F.  H.  Edgeworth, 
ihid.,  aSTovember,  1906.  Easterbrook,  ibid.,  January,  1907  ;  Landois 
Physiologij,  10th  edition,  1904,  p.  810.  G.  S.  Haynes,  Bio-Cliemical 
Journ.,  vol.  i.,  No.  2,  February,  1906.  E.  A.  Lundie,  The  Ophthal- 
mic Renew,  May,  1906.  Mott,  Gihsona  Text-Book  of  Med.,  vol.  ii., 
p.  710.  Gamier  et  Thaon,  Journ.  de  Physiol.,  etc.,  15  Mars,  1906, 
p.  2-52.  Bastian  quoting  Daly,  Allbutt's  System  of  Medicine, 
vol.  vii.,  p.  416.  Leonard  Hill,  The  Cerebral  Circulation,  1896. 
A.  Mosso,  Turin,  Fatigue,  Eng.  translation,  1904. 


190 


CHAPTER  XVII 

CONCLUSION 

It  seems  to  me  to  be  desirable  as  a  conclusion  to  this  study 
of  arteries  and  of  blood-pressure  to  join  together  the  various 
links  into  such  a  chain  as  they  form  in  my  mind.  The 
value  or  strength  of  the  individual  links  will  be  differently 
appraised  by  different  minds  ;  and  some  of  the  links  will 
doubtless  yet  be  strengthened.  I  have,  however,  no  doubt 
they  form  a  chain  sufiiciently  strong  to  serve  as  a  safe  and 
useful  clinical  guide  to  those  not  strongly  committed  to  other 
views. 

To  myself  the  links  naturally  assume  a  chronological 
order, — chronological  as  regards  their  evolution  in  my  own 
mind,  while  such  an  order  does  not  appear  to  be  in  any 
considerable  sense  disadvantageous. 

The  first  link  in  the  chain  is  the  clinical  assurance  that 
the  tightening  up  and  relaxation  of  the  radial  artery  is  a  fact 
of  great  clinical  significance.  The  second  is  the  correction 
of  the  common  conception  that  pressure  is  heightened  inside 
all  hypertonically  contracted  vessels. 

It  is  indeed  imperatively  necessary  unequivocally  to 
separate  the  two  factors  of  the  vessel  wall  and  the  contained 
blood.  The  state  of  the  vessel  wall  need  present  no  initial 
difhculty  ;  it  is  either  thickened  or  not  thickened  :  if  thickened, 
the  degree  necessarily  ^'aries,  and  varies  within  wide  limits. 
The  other  point  is  the  blood-pressure  inside  the  vessel.  This 
can  only  be  arrived  at  by  putting  aside  all  preconceived  ideas 
of  what  is  S'liiyposed  to  happen,  or  ought  to  happen,  when  vessels 
are  thickened.  The  question  of  pressure  inside  the  artery 
has  to  be  approached  from  the  simple  standpoint  of  observa- 
tion made  by  the  cultivated  finger.  That  the  finger  can  do 
this  is  testified  to  by  generations  of  skilled   clinicians  taking 

191 


CONCLUSION 

the  pulse  as  the  test  of  heart  power,  and  if  the  test  of  heart 
power,  necessarily  of  the  blood-pressure  inside  the  vessels. 
This  being  so,  the  controversies  as  to  the  meaning  of  the 
words  tension  and  elasticity  are  merely  of  academic  interest, 
for  they  do  little  or  nothing  to  simplify  the  clinical  position. 
The  less  involved  the  question  can  be  made,  the  more  likely 
is  the  individual  judgment  to  be  correct,  and  in  a  medical 
school  the  student  and  future  practitioner  has  to  be  con- 
sidered. To  be  able  to  estimate  the  pressure  inside  the 
artery,  no  matter  what  the  thickness  of  its  w^all,  is  the  lesson 
to  be  learned,  and  the  learning  of  it  is  to  be  kept  steadfastly 
in  view.  That  it  can  be  attained  is,  to  my  mind,  unquestion- 
able. It  was  never  seriously  questioned  until  the  wrong 
interpretation  of  htemomanometer  readings  was  supposed  to 
discredit  the  value  of  the  sense  of  touch. 

Thickness  of  the  vessel  w^all  is  easy  to  recognise.  The 
thickness,  as  it  varies  in  the  twenty-four  hoars,  and  in 
different  conditions  or  diseases,  is  also  soon  recognised,  when 
the  fact  of  its  occurrence  is  deemed  worthy  of  attention.  It 
will  then  be  found  that  sclerosed  vessels  as  well  as  normal 
vessels  vary  in  thickness.  The  thickeniDg  will  be  found 
associated  with  all  the  causes  which  have  been  enumerated, — 
sometimes  it  is  a  nervous  reflex,  more  commonly  it  is  the 
result  of  blood  impurity.  It  is  a  great  step  to  recognise 
clinically  that  not  only  normal  but  sclerosed  vessels  tighten 
up  and  relax,  for  it  at  once  takes  away  the  conception  of 
the  rigid  tube. 

Having  settled  these  points,  the  next  point  is  to 
determine  what  is  meant  by  the  diffuse  arterio-sclerosis, 
which  was  described  as  if  it  were  atheroma.  The  solution 
of  this  was  sought  for  in  the  radial  artery,  as  it  is  the 
condition  of  that  vessel  during  life  which  leads  to  the 
diagnosis  of  arterio-sclerosis.  The  changes  found  in  the  radial 
and  other  arteries  have  been  described,  and  my  contention 
was  and  is,  that  the  condition  is  not  only  totally  different 
from  atheroma,  but  that  the  changes  in  themselves  clearly 
indicate  their  true  nature. 

The  continued  irritative  stimulation  of  the  arterial  wall, 
manifested  clinically  in  the  sustained  or  recurring  hypertonic 
contraction,   leads   inevitably   to    such    structural   changes    as 

192 


CONCLUSIOxN 

have  been  described.  The  fact  that  a  fibrous  hyperplasia 
of  the  tunica  intima  takes  place,  at  once  shows  that  the 
vessel  changes  are  not  to  be  attributed  to  a  mere  nerve 
influence,  but  to  the  blood  itself.  The  intensity  of  the 
intimal  changes  inside  the  kidneys  appear  to  me  to  clearly 
indicate  the  prolonged  presence  of  excrementitious  substances 
in  the  blood  seeking  an  outlet  by  their  usual  channel.  Here, 
in  short,  lies  the  solution  of  the  problems  as  to  renal, 
cardiac,  and  arterial  changes.  Long-continued  blood  con- 
ditions preceded  the  vascular,  cardiac,  and  renal  changes  so 
well  known.  If  the  kidney  itself  was  the  seat  of  a  primary 
inflammation  of  the  subacute  type,  the  blood  condition 
necessarily  resulting  led  to  the  widespread  changes  of  arterio- 
sclerosis and  heart  hypertrophy.  The  development  of  heart 
hypertrophy  as  a  result  of  the  raising  of  aortic  pressure  has 
not  appeared  to  me  to  require  to  be  dealt  with  here. 

After  the  recognition  of  these  facts,  the  problem  of  blood- 
pressure,  as  it  was  estimated  by  the  clinician  and  thought 
of  by  the  physiologist,  presented  great  difficulty.  The 
sphygmograph,  the  arteriometer,  the  hsemodynamometer  of 
Oliver,  an  occasional  use  of  the  Eiva-Eocci  sphygmometer, 
did  not  seem  to  me  to  help  the  solution  of  the  problem. 
The  advent  of  the  modifications  of  the  Eiva-Eocci  instrument 
led  to  a  more  sustained  use  of  them,  and  the  results  when 
placed  alongside  the  evidence  obtained  by  the  sense  of  touch 
seemed  to  be  hopelessly  conflicting.  Amongst  one's  friends 
or  colleagues  the  same  conflicting  evidence  was  available ; 
some  allowed  the  manometer  to  supplant  their  ancient  faith 
in  the  sense  of  touch,  others  treated  the  evidence  afforded 
by  the  instruments  with  a  neglect  bordering  on  contempt. 
The  same  diversity  of  view  seemed  to  prevail  widely.  My 
solution  of  the  problem  has  been  presented  in  the  preceding 
chapters.  The  condition  of  the  arterial  wall  has  been  shown 
to  be  the  added  factor  causing  the  high  hsmomanometer 
readings  obtained  in  pathological  conditions.  The  state  of 
the  arterial  wall,  and  the  relation  of  its  thickness  to  the 
size  of  the  lumen,  is  determined  not  only  by  permanent 
structural  thickening,  but  by  the  thickening  of  hypertonic 
contraction.  The  steps  from  hypertonus  to  sclerosis  of 
vessels  and  arterio-sclerotic  granular  kidney  have  been  indi- 
N  193 


CONCLUSION 

cated ;  the  causes  of  hypertonus  have  been  examined,  and 
it  has  been  shown  that  the  direct  influence  of  the  blood 
composition,  upon  the  vessel  wall  must  have  a  predominant 
place  given  to  it  in  this  connection.  Experimental  data 
and  all  clinical  experience  are  available  in  support  of  this 
generalisation. 

I  need  not  add  to  the  length  of  this  monograph  by 
adding  a  special  chapter  on  treatment.  In  various  of  the 
preceding  chapters  I  have  dealt  with  treatment  and  pre- 
vention sufficiently  to  indicate  the  lines  I  follow.  I  shall 
only  repeat  that  the  aim  is  to  prevent  hypertonic  contrac- 
tion. If  the  vessels  are  already  sclerosed,  the  prevention  of 
hypertonus  will  often  prevent  the  loss  of  the  faculties  the 
possession  of  which  makes  life  worth  living.  To  those  who 
are  well  on  in  life  and  do  not  enjoy  the  readings  of  the 
hfemomanometer,  there  is  abundant  solace  available  in  the 
abandonment  of  the  idea  that  blood-pressure  rises  with 
advancing  life.  Even  if  arteries  are  permanently  thick,  life 
need  not  be  materially  shortened  if  hypertonus  be  prevented, 
and  if  steps  be  taken  to  allay  arterial  irritability ;  and  these 
are  undoubtedly  within  our  control.  If  hypertonic  contraction 
be  avoided  there  need  be  no  fear  of  cerebral  haemorrhage  as 
life  advances.  The  changing  tonus  of  the  thickened  vessels 
can  be  followed  by  the  hfemomanometer,  and  the  records  cor- 
rectly interpreted  are  a  valuable  guide  to  prophylaxis.  The 
instrument  ought,  however,  to  be  called  the  Angiomanometer 
when  used  as  an  instrument  in  clinical  pathology,  for  the 
clinician  must  recollect  that,  given  thickened  vessels,  the 
instrument  records  not  blood-pressure,  but  arterial  resist- 
ance. 


194 


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